Alzheimer's treatment and prevention

[mr peabody]

Benzodiazepine use may increase the risk of Alzheimer’s disease

By Beverly Merz

If you have ever taken Valium, Xanax, or some other benzodiazepine to calm your nerves or sleep better, you may have felt woozy or hungover the next day. Experts have long assumed that people’s heads would clear once they stopped taking the drug. That may not be the case. A study published by the journal BMJ suggests that benzodiazepine use may promote the development of dementia.

A team of researchers from France and Canada linked benzodiazepine use to an increased risk of being diagnosed with Alzheimer’s disease. In the study, the greater a person’s cumulative dose of benzodiazepines, the higher his or her risk of Alzheimer’s.

The association isn’t surprising given past research on the subject, but it still should be viewed with caution. “Benzodiazepines are risky to use in older people because they can cause confusion and slow down mental processes,” says Dr. Anne Fabiny, chief of geriatrics at Harvard-affiliated Cambridge Health Alliance. “However, although there is an association, we still can’t say that benzodiazepines actually cause Alzheimer’s,” she cautions.

Dose, duration, and type of drug matter

The researchers relied on a database maintained by the Quebec health insurance program. From it, they identified nearly 2,000 men and women over age 66 who had been diagnosed with Alzheimer’s disease. They randomly selected more than 7,000 others without Alzheimer’s who were matched for age and sex to those with the disease. Once the groups were set, the researchers looked at the drug prescriptions during the five to six years preceding the Alzheimer’s diagnosis.

People who had taken a benzodiazepine for three months or less had about the same dementia risk as those who had never taken one. Taking the drug for three to six months raised the risk of developing Alzheimer’s by 32%, and taking it for more than six months boosted the risk by 84%.

The type of drug taken also mattered. People who were on a long-acting benzodiazepine like diazepam (Valium) and flurazepam (Dalmane) were at greater risk than those on a short-acting one like triazolam (Halcion), lorazepam (Ativan), alprazolam (Xanax), and temazepam (Restoril).

The researchers acknowledge that the use of benzodiazepines could be just a signal that people are trying to cope with anxiety and sleep disruption—two common symptoms of early Alzheimer’s disease. If that’s true, their use of a benzodiazepine may not be a factor in causing dementia but an indication it is already in progress.

Other reasons to avoid benzodiazepines

Even if that’s so, there are other reasons for older people to avoid benzodiazepines. In 2012, the American Geriatrics Society added benzodiazepines to their list of inappropriate medications for treating insomnia, agitation, or delirium. That decision was made primarily because common side-effects of benzodiazepines—confusion and clouded thinking—often have disastrous consequences, including falls, fractures, and auto accidents.

Even short-acting benzodiazepines pack a bigger punch in older people. As the body’s metabolism slows with age, drugs take longer to clear. And because benzodiazepines are stored in body fat, they can continue to produce effects days after people stop taking them.

Although these medications are taken to help people get a good night’s rest, they can have the opposite effect. “When they’re taken over time, they can actually interfere with normal sleep,” says Dr. Fabiny. The quest to sleep through the night can lead to prescriptions for higher doses or longer-lasting benzodiazepines—and even greater side effects.

If you are a caregiver for an older person, you may want to check the medicine cabinet. If you find benzodiazepine, you might want to discuss it with him or her, or with a doctor.

If you take a benzodiazepine, keep in mind that these drugs are designed for short-term use. If you’ve been using them regularly for more than a few weeks, know that withdrawal symptoms can be powerful. Consider talking to your doctor about alternatives.

There’s currently no cure or treatment for Alzheimer’s disease. That makes prevention all the more important. Limiting the use of a benzodiazepine for anxiety or sleep troubles may be one small step toward prevention.

https://www.health.harvard.edu/blog...ay-raise-risk-alzheimers-disease-201409107397

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Deep brain stimulation (DBS) of Alzheimer's patients

When neuropsychologist Gwenn Smithwas on staff at the University of Toronto, she worked on deep brain stimulation of Alzheimer’s patients with neurosurgeon Andres Lozano.
DBS, in which a medical device is implanted into the brain to stimulate a particular circuit, is used to control tremors in Parkinson’s disease and is under investigation for managing depression
and chronic pain, but its application in Alzheimer’s was novel.

For their pilot, in which DBS was tested in six patients to target the fornix, a bundle of nerve fibers involved in brain memory circuits, Smith analyzed PET scans to study cerebral glucose metabolism to assess safety of the DBS procedure. “Usually, over a 1-year course of Alzheimer’s disease, a decrease in metabolism is observed that correlates with memory getting worse,” Smith explains. Instead, their study observed a sustained increase in glucose metabolism of the brain over one year.

After Smith moved to Johns Hopkins in 2008, she suggested Lozano as the inaugural speaker for the Michael M. Ossoff Visiting Lectureship in Memory Disorders and Alzheimer’s Disease, and introduced Lozano to psychiatrist Constantine Lyketsos. The trio collaborated on a multi-center phase II study of DBS in 42 Alzheimer’s disease patients, further demonstrating safety and a potential benefit for patients over age 65. The study group included an interdisciplinary team of psychiatrists, neurologists, neurosurgeons and neuropsychologists. The work, published last fall in the Journal of Alzheimer’s Disease, was also presented at the Alzheimer’s Association International and Clinical Trials on Alzheimer’s Disease conferences in 2015.

Their study enrolled patients ages 45-85 with mild Alzheimer’s disease. All had caregivers who could reliably report their activities and functioning, and all were taking a stable dose of a cholinesterase inhibitor medication. After the participants were implanted with electrodes, half were randomly assigned to receive continuous stimulation for one year, while the other half received no stimulation. Investigators measured cognitive function and cerebral glucose metabolism.

"Although there were no differences in cognitive outcomes for participants as a whole, in analyses limiting the sample to those 65 and older," says Smith, “there was a trend for cognitive benefit, or even stability, in the older Alzheimer’s patients who were treated with DBS. They showed greater increases in cerebral glucose metabolism, compared with the older patients not treated with DBS. This was not seen in the younger patients.”

Additional analyses of the data are ongoing, some suggesting that stimulation may cause an increase in the volume of the hippocampus, where early Alzheimer’s pathology surfaces.

It’s not clear why younger patients didn’t fare as well. “We hypothesize that an effect in younger patients would be more difficult to detect because both glucose metabolism and cognition decline more rapidly than in older patients,” says Smith. still, “the sense is the treatment is still worth pursuing, but we need to learn more about how to optimize DBS for individual patients, as is well established in Parkinson’s.”

In Parkinson’s disease, clinicians implanting electrodes can determine which contact is more effective by testing the contacts and seeing immediately that if they stimulate in a particular place, tremors stop. In Alzheimer’s disease, explains Smith, it’s not that simple: “We need to develop methods to detect short-term improvement in memory, which is challenging. We also need to learn more about the mechanisms of action of DBS so that we can develop biomarkers to predict treatment response.”

The team is working to define parameters for its next study. Their study enrolled patients ages 45-85 with mild Alzheimer’s disease. All had caregivers who could reliably report their activities and functioning, and all were taking a stable dose of a cholinesterase inhibitor medication. After the participants were implanted with electrodes, half were randomly assigned to receive continuous stimulation for one year, while the other half received no stimulation. Investigators measured cognitive function and cerebral glucose metabolism.

"Although there were no differences in cognitive outcomes for participants as a whole, in analyses limiting the sample to those 65 and older," says Smith, “there was a trend for cognitive benefit, or even stability, in the older Alzheimer’s patients who were treated with DBS. They showed greater increases in cerebral glucose metabolism, compared with the older patients not treated with DBS. This was not seen in the younger patients.”

Additional analyses of the data are ongoing, some suggesting that stimulation may cause an increase in the volume of the hippocampus, where early Alzheimer’s pathology surfaces.

It’s not clear why younger patients didn’t fare as well. “We hypothesize that an effect in younger patients would be more difficult to detect because both glucose metabolism and cognition decline more rapidly than in older patients,” says Smith. Still, “the sense is the treatment is still worth pursuing, but we need to learn more about how to optimize DBS for individual patients, as is well established in Parkinson’s.”

In Parkinson’s disease, clinicians implanting electrodes can determine which contact is more effective by testing the contacts and seeing immediately that if they stimulate in a particular place, tremors stop. "In Alzheimer’s disease," explains Smith, "it’s not that simple: We need to develop methods to detect short-term improvement in memory, which is challenging. We also need to learn more about the mechanisms of action of DBS so that we can develop biomarkers to predict treatment response.”

The team is working to define parameters for its next study.

-hopkinsmedicine.org

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Ayahuasca stimulates the birth of new neurons

Studies carried out by the Beckley/Sant Pau Research Program have revealed that ayahuasca use can result in an increase in several key traits associated with mindfulness, such as ‘decentering’, which refers to the ability to observe one’s thoughts and feelings in an objective and non-judgmental way. This, in turn, has been shown to help sufferers of depression, anxiety, grief and PTSD to overcome their conditions.

Brain-imaging studies have revealed how ayahuasca reduces the control of a brain network called the default mode network, and provide compelling evidence that this may be behind the brew’s therapeutic power. Intriguingly, certain compounds in ayahuasca stimulate the birth of new neurons from stem cells in a petri dish. This opens the door to the possibility of using ayahuasca to regenerate damaged brain cells, potentially pointing the way to a new pathway to treating Alzheimer’s and dementia.

-Beckley

 

[mr peabody]

Cannabinoides reduce inflammation, restore cognitive function

Alzheimer’s appears because of inflammation in the brain, and the brain’s inability to remove amyloid beta plaque.

Gary Wenk, Ph.D, professor of neuroscience, immunology and medical genetics at Ohio State University, on marijuana and its link to inflammation:

“I have been trying to find a drug that will reduce brain inflammation and restore cognitive function in rats for over 25 years; cannabinoides are the first and only class of drugs that have ever been effective.”

You know what plaque on your teeth is because of your dentist. He or she tells you to clean your teeth so they won’t be left covered in plaque.

You can watch the dentist scrape plaque off, but what about brain plaque?

Brain plaque is the common term for acetylcholinesterase-associated amyloid β-peptide (Aβ). We can’t see this get wiped away, and even if we could, we wouldn’t. This is because our brains clear themselves out while we’re asleep.

Marijuana helps protect against brain inflammation, which in turn aids in the brain’s waste removal process. Unlike other Alzheimer’s medications, marijuana has been proven to work, does not demean or insult patients, costs considerably less to produce, and eases the brain, mind, and soul.

-Michelle Toole

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"Psychedelic room" helps dementia patients

For many people living with conditions such as Alzheimer's disease, this is a daily reality. Now, psychologists are reaching back to the 1960s and updating research on sensory deprivation with the hope of offering relief to people suffering from this type of dementia.

What looks like a modern art exhibit is in fact a room that enhances mental stimulation for people with dementia. Colored lights, a giant butterfly, and a tube filled with bubbles are just some of the objects that fill the space.

The treatment, which originated in the Netherlands and is called Snoezelen (pronounced snooze-lin), was originally used to help children suffering from autism. Previous research has shown that Snoezelen behavior therapy "reduces socially disturbed behavior, produces relaxation responses, improves mood enhances interpersonal interaction, facilitates verbal expression, improves memory recall, and enhances attention and concentration in dementia patients," said lead researcher Dr. Jason Staal of Beth Israel Medical Center in New York City.

"Everything is done to maximize the wonderful joy of the experience. Remember these are people living in monochromatic, sensory deprived environments," Staal told Reuters Health, referring to bleak hospital rooms and the like. "The aim is to provide dementia patients with an experience that they can understand."

Dementia patients often lose the ability to read or understand words and the ability to complete tasks like preparing a meal or finding their shoes and putting them on. Music and color preference, on the other hand, tend to remain intact longer, explained Staal. For instance someone who likes the color blue will most likely have the same color preference into old age, even when dementia comes into play.

Patients are exposed to the room anywhere from three to five times per week depending on their degree of dementia. Two therapists accompany them, one who assists the patient in the room and another who other acts as an observer. At first the patient is closely monitored to see which stimuli have the most positive effect. The therapist is then able to focus and heighten the patient's experience in subsequent visits into the room.

"The current state of affairs in the day-to-day treatment for people with dementia is pretty miserable," said Staal.
-Reuters

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Ayahuasca and neurogenisis

New research shows the drug stimulates the generation of human neural cells that block the effects of DYRK1A, a gene that is overactivated in Alzheimer's and Down syndrome patients.

One of the main substances present in the Ayahuasca beverage is harmine, a beta-carboline which potential therapeutic effects for depression has been recently described in mice.

In order to elucidate these effects, researchers from the D'Or Institute for Research and Education (IDOR) and the Institute of Biomedical Sciences at the Federal University of Rio de Janeiro (ICB-UFRJ) exposed human neural progenitors to this beta-carboline.

After four days, harmine led to a 70 percent increase in proliferation of human neural progenitor cells.

Researchers were also able to identify how the human neural cells respond to harmine.

The described effect involves the inhibition of DYRK1A, which is located on chromosome 21 and is over activated in patients with Down syndrome and Alzheimer's Disease.

-Mia De Graaf

 

[mr peabody]

Coffee may reduce risk of Alzheimer’s and Parkinson’s

Alzheimer’s disease is the most common neurodegenerative disease and a leading cause of dementia.

Studies have shown that coffee drinkers have up to a 65% lower risk of developing Alzheimer’s disease.

Parkinson’s is the second most common neurodegenerative disease and caused by the death of dopamine-generating neurons in the brain.

Coffee drinkers have a 32-60% lower risk of Parkinson’s disease. The more coffee people drink, the lower the risk.

Bottom Line: Several studies show that coffee drinkers have a much lower risk of dementia, Alzheimer’s disease and Parkinson’s disease in old age.

-Kris Gunnars

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I am not aware of any research with MDMA or hallucinogens and Alzheimer's. However, there has been some research on MDMA and Parkinson's that was inspired by case studies of
Parkinson's patients who experienced a dramatic remission of their symptoms after taking ecstasy/MDMA.

-5-HT2

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I believe LSD may have some value in Alzheimer's. Since LSD attenuates the brain's sensory input filter. By allowing more sensory input through, the stunted Alzheimer brain, may get a
"kick-start" if you will? I think this idea should be explored further.

-CaptainRainbow

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I agree, MDMA is probably not the best for a neurodegenerative disease, but I do think there's a chance theoretically that LSD, or psilocybin (or DMT) could help seeing as how they tend to upregulate BDNF and promote neurogenesis and new synaptic spines. I always think a good way to combat neurodegeneration, is with neurogenesis. Also atleast with ayahuasca, it's been found to increase SERT platelets in the serum.

-poneelovesyou

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5-HT2A and mGlur3 exist as antagonistic heterodimers, meaning, activation of one will oppose the other, inhibition of one will enhance the other. If that's the dominant interaction you wouldn't really expect a catastrophic effect. For any other class of drug we would just test for these effects; with research censored we just have to wonder what might happen. I think the success of MDMA for PTSD should at least get us interested in finding other areas we can use these drugs.

-endotropic

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Memantine is used to treat Alzheimer’s disease, and it may be useful in treating mild to moderate cases of vascular dementia. Memantine is the first representative of a new class of Alzheimer’s drugs—a moderate affinity NMDA-receptor antagonist. It has been touted as improving cognitive and psychomotor functioning, providing benefits in the activities of daily living, reducing the dependance on outside care, and is said to have a good tolerability. It is also believe to have neuroprotective effects (by preventing the influx of calcium due to blocking the NMDA receptor in the presence of sustained release of low glutamate concentrations) at the dosages used in treating Alzheimer’s disease (which could slow the progression of the disease). The maximum daily amount recommended to treat Alzheimer’s is 20 mg.

-memantine.com

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The ability of hallucinogens such as LSD to interact with receptors for endogenous neurotransmitters such as GABA, serotonin and glutamate is significant. LSD and other psychedelics can modulate activity in the Default Mode Network. This is a distinct network of brain regions providing the neurologic basis for “self.” Abnormal function in this network may be responsible for disorders such as autism, Alzheimer’s, PTSD, chronic pain and certain depressive disorders. In addition to providing possible mechanisms explaining microdosing’s clinical actions in regulating mood, these findings point to important research possibilities.

-Dr. Bruce Heischober

 

[mr peabody]

Many people develop tics while on Dopaminergic medications/drugs, but that doesn't necessarily mean that damage has been done. Dopamine is important for movement and generally
too much dopamine means too much movement, I would look at the movement disorders associated with the L-dopa.

MDMA might possibly have a correlation to dementia (time will tell how significant) but not to Parkinson's. Cocaine users seem to be doing just fine from what other blue lighters have said.

There is a solid connection between anticholinergics and dementia, so I think excess acetylcholine would be okay. Not that I'm sure excess acetylcholine is the problem. If that were the case
I would assume people on acetylcholinesterase inhibitors or colouracetam and such would have problems with excess movement, which I haven't heard about.

The pathology of fasciculations is probably different than tics though by the way.

-Cotcha Yankinov

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The damage to serotonergic axons caused by Ecstasy is very similar to those seen in Alzheimer's Disease. In both cases, the loss of certain presynaptic serotonergic receptors and abnormal levels of the chemical acetylcholine is what is responsible for the hallucination or dementia that the person experiences. Although it is not exactly clear if the use of amphetamines and drugs
like Ecstasy cause adverse effects, it is clear that MDMA does have the potential to cause neurotoxicity.

Drugs such as Ecstasy and other such amphetamine that deplete the chemical serotonin in the brain cause alterations in mood and behavior, resulting in a more euphoric state for the user.
As in any drug, the mood elevations and distorted sense of reality is a result of an imbalance in the different chemical processes in the brain that is being effected by the drug.

-Maureen Kyin

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MDMA increases risk of brain damage and eventual Alzheimer's

By Denis Campbell

Dutch researchers found that ecstasy users had an increased risk of hippocampal damage, which can contribute to the eventual onset of Alzheimer's.

Long-term Ecstasy users risk brain damage, memory loss and an increased chance of developing Alzheimer's disease, new research suggests. Dutch researchers used MRI scans to study the brains of 10 men in their mid-20s who had taken an average of 281 ecstasy tablets over the previous six and a half years, and seven peers who had taken other drugs.

They found that the hippocampus - the part of the brain controlling memory - was 10.5% smaller among the ecstasy users, and their overall grey matter 4.6% less.

"These data provide preliminary evidence that MDMA users may be prone to incurring hippocampal damage", and may help explain the memory loss witnessed among such people in previous studies, the co-authors wrote in the Journal of Neurology, Neurosurgery and Psychiatry.

"Hippocampal atrophy is a hallmark for disease of progressive cognitive impairment in older patients, such as Alzheimer's disease", they added.

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New MDMS users who took ten or more ecstasy pills over their first year of use showed decreased function of their immediate and short-term memory compared with their pre-ecstasy performance. These findings are associated with damage of the hippocampus, the area of the brain that oversees memory function and navigation. Interestingly, hippocampal damage
is one of the first signs of Alzheimer's disease, resulting in memory loss and disorientation.

-Wiley

 

[mr peabody]

Is Alzheimer's a form of diabetes?

The accumulated evidence is now so strong that many specialists are comfortable referring to Alzheimer's as type 3 diabetes.

Insulin doesn't merely signal the body's somatic cells to take up glucose; it also governs the brain's uptake of glucose. And glucose is what powers the brain. It's the brain's primary energy molecule.

We've known for some time that the brain itself makes a certain amount of insulin, and various parts of the brain are rich in insulin receptors. It's also well established that cognitive decline
is correlated with both obesity and metabolic abnormalities involving insulin.

Dr. David Perlmutter lays the blame squarely on diet, and details the case for eating more fats and cholesterol (yes, more cholesterol) and cutting gluten from your diet entirely, pointing to studies that have linked low cholesterol to cognitive impairment.

-Kas Thomas

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Studies carried out by the research team at Warren Alpert Medical School at Brown University identified the possibility of a new form of diabetes after finding that insulin resistance can
occur in the brain.

Lead researcher, Dr Suzanne de la Monte, carried out a further study in 2012 to further investigate the link.

The researchers pinpoint resistance to insulin and insulin-like growth factor as being a key part of the progression of Alzheimer’s disease.

Whereas type 1 and type 2 diabetes are characterized by hyperglycemia (increased blood sugar), a separate study, carried out by the University of Pennsylvania and published in 2012, excluded people with a history of diabetes, indicating that Alzheimer’s can develop without the presence of significant hyperglycemia in the brain.

People that have insulin resistance, in particular those with type 2 diabetes have an increased risk of suffering from Alzheimer's disease estimated to be between 50% and 65% higher.

Researchers have discovered that many type 2 diabetics have deposits of a protein called amyloid beta in their pancreas which is similar to the protein deposits found in the brain tissue
of Alzheimer's sufferers.

-diabetes.co.uk

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New research shows insulin resistance is one of the major factors that starts the brain-damage cascade, which robs the memory of over half the people in their 80s, leading to a diagnosis of Alzheimer’s disease.

Eating sugar and refined carbs can cause pre-dementia and dementia. But cutting out the sugar and refined carbs and adding lots of fat can prevent, and even reverse, pre-dementia and early dementia.

Studies show people with diabetes have a four-fold risk for developing Alzheimer’s. People with pre-diabetes or metabolic syndrome have an increased risk for having pre-dementia or mild cognitive impairment (MCI).

You don’t have to have full blown type 2 diabetes to develop brain damage and memory loss from high insulin levels and insulin resistance.

-Dr. Mark Hyman

 

[mr peabody]

Virus and bacteria identified as major causes of Alzheimer’s

A worldwide team of senior scientists and clinicians have come together to produce an editorial which indicates that certain microbes – a specific virus and two specific types of bacteria
– are major causes of Alzheimer’s Disease. Their paper, which has been published online in the highly regarded peer-reviewed journal, Journal of Alzheimer’s Disease, stresses the urgent need
for further research – and more importantly, for clinical trials of anti-microbial and related agents to treat the disease.

This major call for action is based on substantial published evidence into Alzheimer’s. The team’s landmark editorial summarises the abundant data implicating these microbes, but until now this work has been largely ignored or dismissed as controversial – despite the absence of evidence to the contrary. Therefore, proposals for the funding of clinical trials have been refused, despite the fact that over 400 unsuccessful clinical trials for Alzheimer’s based on other concepts were carried out over a recent 10-year period.

Opposition to the microbial concepts resembles the fierce resistance to studies some years ago which showed that viruses cause certain types of cancer, and that a bacterium causes stomach ulcers. Those concepts were ultimately proved valid, leading to successful clinical trials and the subsequent development of appropriate treatments.

Professor Douglas Kell of The University of Manchester’s School of Chemistry and Manchester Institute of Biotechnology is one of the editorial’s authors. He says that supposedly sterile red blood cells were seen to contain dormant microbes, which also has implications for blood transfusions.

“We are saying there is incontrovertible evidence that Alzheimer’s Disease has a dormant microbial component, and that this can be woken up by iron dysregulation. Removing this iron will slow down or prevent cognitive degeneration – we can’t keep ignoring all of the evidence,” Professor Douglas Kell said.

Professor Resia Pretorius of the University of Pretoria, who worked with Douglas Kell on the editorial, said “The microbial presence in blood may also play a fundamental role as causative agent of systemic inflammation, which is a characteristic of Alzheimer’s disease – particularly, the bacterial cell wall component and endotoxin, lipopolysaccharide. Furthermore, there is ample evidence that this can cause neuroinflammation and amyloid-β plaque formation.”

The findings of this editorial could also have implications for the future treatment of Parkinson’s Disease, and other progressive neurological conditions.

...

This makes total and complete sense to me. i immediately connected it to the chickenpox/shingles correlation. the possible causes of AD listed in this article are definitely appropriate to my husband. my husband was diagnosed with age related dementia/AD in june 2012 by mri (at age 80, when he was still actively pastoring a church). he had had several mri over a period of years showing progressive plaque build up with some symptomatology. after major open heart surgery in may 2013 there was a major change in his status mentally for the worse and with a slow downhill slide, along with physical weakening, such as in his balance & hearing, even tho he now exercised on a regular basis – something he had not done in more than 30 years. as of january 2016, he is now on dialysis, with another drop in mental status. he lost a sister diagnosed with AD in april 2015 at the age of 95 and has a sister with mild dementia who just reached the age of 99. we did almost not accept going on the dialysis due to the AD, even knowing it would have meant imminent death. living with this disease on a daily basis, the current ‘meds’ for it are worse than the disease itself, are too expensive, & many times of no use. we need to find a way to stop this disease. these clinical trials must be funded. the treatments are there for us to find & are probably already on our shelves now.

-redhvn56

...

In the editorial of the Journal of Alzheimer Disease , published in 8 March 2016 with the title “MICROBES AND ALZHEIMER’S DISEASE”,the dozens of prestigeous researchers of prestigeous universtities of dozens of countries around the world that wrote the milestone text of it very interesting editorial , agree that herpes simplex virus type 1 , Chlamydia pneumoniae, and several types of spirochaete (as Borrelia of Lyme disease) , fungal infections,etc. can be related as some triggers (but NOT as causes) of Alzheimer disease.Extra Virgin Coconut Oil is empirically used as mitochondrial function improver and as alternative fuel to the brain in AD and others dementias , still without scientific foundation, but with hundreds of empirical testimonies by patients , caregivers and relatives of patients that gives some improve in dementias as AD.

-Carlos Oliveira

...

The findings that AD has a microbial etiology is indeed a significant finding. Microbiologists can possibly try using probiotics for the prevention and treatment of AD. Recent research outputs have shown that the human intestinal microbiome composition plays an important role in orchestrating the overall health and well-being of an individual. Probiotics have already been used for the prevention of certain nutritional deficiencies, hyperlipidemia, colorectal cancer and hopefully even diabetes.

-Teddy Quark

...

This may be a situation where the infecting/offending organism does the damage to start the process in motion and once established antimicrobial therapy is not effective. Examples include Hepatitis C or B virus where treated early causes limited liver damage but over time may lead to cirrhosis or liver cancer. At that later time treating the virus is too late. Trials might want to focus on very early AD or better yet if one can make the definite link between an organism and AD treat before symptoms develop. As a microbiologist I believe it warrants much more study.

-Ray

...

Two Spriochetal Infections -

Borrelia spirochetes ( Blood and Tissue pathogens) Transmitted by insect bites
Treponemal spirochetes from the oral cavity ( Periodontal disease pathogens)

are linked to Alzheimer’s Disease pathogenesis.

I offer in support of the Chronic Borrelia spirochete brain infections in Alzheimer’s disease, the following two links to lectures which describe images of the
Borrelia in Autopsy Alzheimer’s Brain tissue from the Harvard Medical School Brain Bank.
—
Link:; Original 37 min Powerpoint without narration:
https://www.dropbox.com/s/nthxi50bt... Borrrelia Narrated for Translation.pptx?dl=0
—
Link:: Video with Narration 44 min.:
Final Lecture German Borreliosis Society Alan B MacDonald Lecture March 11 2016

Borrelia brain infections provide the most Photographic documentation of The Cause of Alzheimer’s Disease, as proven by direct Photographs of these microbes by DNA probe imaging
in autopsy Alzheimer’s disease Brains.

-Alan B. MacDonald, MD

...

This is an interesting article. I think fundings for the clinical trials should be instituted in other to proof or disproof this relationship between infection and AD. There have been many funded clinical trials on AD and other concepts which showed little or no evidence. So i see no reason why this concept should not also be funded for clinical trials. For as realised, the most promising concepts are always initially rejected, and they only come to realise that many years later. For example, the idea of the scientist who said peptic ulcer was caused by a bacterium was rejected until he had to proved it himself by drinking a cork-tail of the bacterium which is not suppose to be that way.

-Alan B. MacDonald

 

[mr peabody]

Alzheimer’s: The early warning sign everyone should know

This Alzheimer’s early warning sign could provide a way of warding off the neurodegenerative disease.

Poor sleep could be an early sign of Alzheimer’s in people who are otherwise healthy, new research finds.

Scientists have found links between certain biological markers of Alzheimer’s and sleep disturbances. Dr Barbara B. Bendlin, who led the study, said:

“Previous evidence has shown that sleep may influence the development or progression of Alzheimer’s disease in various ways.For example, disrupted sleep or lack of sleep may lead to amyloid plaque buildup because the brain’s clearance system kicks into action during sleep. We looked not only for amyloid but for other biological markers in the spinal fluid as well.”

The study was carried out on 101 people with an average age of 63. All were at risk of Alzheimer’s, although none had any symptoms. The results showed that those with the worst sleep quality also had biological markers of Alzheimer’s in their spinal fluid. Dr Bendlin said:

“It’s important to identify modifiable risk factors for Alzheimer’s given that estimates suggest that delaying the onset of Alzheimer’s disease in people by a mere five years could reduce
the number of cases we see in the next 30 years by 5.7 million and save $367 billion in health care spending.”

Not everyone with sleep problems had the biological markers, though, said Dr Bendlin:

“It’s still unclear if sleep may affect the development of the disease or if the disease affects the quality of sleep. More research is needed to further define the relationship between sleep
and these biomarkers. Improving sleep could be one way of helping to ward off Alzheimer’s," said Dr Bendlin. "There are already many effective ways to improve sleep. It may be possible
that early intervention for people at risk of Alzheimer’s disease may prevent or delay the onset of the disease.”

 

[Regaining_My_Soul]

I take:

• Acetyl-L-Carnitine
• Fisetin
• Benfotiamine
• Nicotinamide Riboside
• Huperzine-A

for Alzheimer's/dementia prevention

 

[mr peabody]

Natural substances extracted from the ayahuasca plants have been found to possess unique restorative and strongly antioxidative properties on specific nerve cells in the brain and central nervous system – controlling neurotransmission, muscle/motor activity, memory and coordination. This gives probable cause to the theory that ayahuasca could be an effective treatment for neurodegenerative diseases such as ALS, Alzheimer’s, and Parkinson’s disease. Promising results as of date has also been obtained from studying the substance psilocybin, very closely related to the substances found in ayahuasca, naturally occuring in certain species of medicinal mushrooms consumed by the indigenous people where ayahuasca is also used.

According to Dr. Juan Ramos, head of the neurological disease department at the South Florida university, USA, initial studies show that these substances stimulate the development of new cells in the areas of the brain controlling the above mentioned functions. If this could prove to be an eventual cure through complete restoration of damaged or destroyed cells remains to be seen, but initial results indicate this could potentially be the case. There is also a growing interest in exploring the cell regenerative properties of these plants within the spinal chord injury support communities. Should people with this background eventually try and find the results of this treatment useful, medical science would be bound to take note. Cancer researchers have also shown interest in B. Caapi, as its different alkaloids has shown to be effective against the growth of cancer cells.

Summary

Ayahuasca could effectively be used in treatment of ALS and other motor neuron diseases based on the fact that studies suggest uniquely antioxidative effects that seem to protect brain/nerve cells, targeting motor neurons through a unique biochemical transport system, and that it and other molecularly similar substances, also naturally occurring, stimulate neurogenesis – the development of new brain/nerve cells, and the communicative capacity between these. In studies it has been found to reduce symptoms in Parkinson’s patients – all neurodegenerative diseases share common ground, thus making it likely that something that improves a given neurological condition could also be beneficial to other conditions nearly related. Also based on credible personal accounts from people having used ayahuasca for symptom relief from their multiple sclerosis (once again – the common ground of neurodegenerative diseases), documented in books about ayahuasca, and from descriptions of early stage minor improvement by those with various types of ALS now participating in the treatment project, already having used this medicine for a period of time. Studies also indicate ability to normalize metabolism in mitochondria, crucial to motor neuron survival, and to regulate and decrease levels of excitotoxicity in the central nervous system.

-Daniel Gustafsson

-----

Psychedelic tea from the Amazon stimulates brain cells and could treat Alzheimer’s

By Olivia Lerche

SCIENTISTS have discovered that a hallucinogenic substance from the Amazon stimulates the birth of new brains cells and could lead to treatment for neurodegenerative diseases
such as Alzheimer’s disease. The tea called Ayahuasca, is also used as a traditional spiritual medicine in ceremonies in Peru, South America.

The Sant Pau Hospital Barcelona, which worked in collaboration with the Beckley Foundation and Spanish National Research Council in Madrid, has released the findings from a study investigating the potential of ayahuasca to promote neurogenesis - which is the development of new brain cells. The investigators believe that these findings will open up a new avenue of research that may help develop drugs to treat diseases like Alzheimer’s, Parkinson’s and addiction.

Dr Jordi Riba, lead investigator, presented preliminary data, at the Interdisciplinary Conference on Psychedelic Research in Amsterdam at the weekend. Results showed that two compounds - harmine and tetrahydro harmine - which are found in the hallucinogenic tea, potently stimulated the transformation of stem cells into new neurons.

Amanda Feilding, director of the Beckley Foundation said: “The images from the Beckley/Sant Pau collaboration showing the birth of new neurons are very interesting and suggest that ayahuasca could lead to a new approach in the treatment of neurodegenerative conditions such as Alzheimer’s and Parkinson’s, among others.”

Experts have believed for years that the brain doesn’t make neurons during adulthood. In the 1990s, research changed this finding, showing that new neurons are generated throughout adult life in two regions of the human brain: the area around the ventricles and in the hippocampus. The hippocampus, thought to be the center of emotion and autonomic nervous system, plays a key role in memory. Its function declines with age and in neurological disorders.

Under normal conditions, the rate of the birth of new neurons is very low, and it cannot keep up with the rate of neural death that occurs in diseases such such as Alzheimer’s disease. In the study, neural stem cells were isolated from the hippocampus of adult mice. The stem cells were grown in the lab and substances that are present in ayahuasca were added to the cultures and compared with saline a placebo control.

Scientists have described the results as ‘impressive’, with ayahuasca substances stimulating the transformation of stem cells into new neurons.

Dr Riba has been studying ayahuasca for twenty years.

 

[Abject]

I've come across AD being referred to as Type III Diabetes, being the result of insulin resistance of the brain. I can certainly see hypometabolism/mitchondrial dysfunction being integral to AD.

 

[Thewhirerabbit333]

Dxm has been making leaps and bounds in neurological treatments and for good reasons. People need to put away that negative perspective for a second and actualy seek medical information instead of clicking the first thing they see saying how bad dxm is.
It's suppressed and mocked for a reason, it's to filer out those who don't take the time to seek www.sciencedirect.com/science/article/pii/S0163725816000176

 

[clubcard]

Association is not cause and effect. Heroin users are more likely to suffer mental health issues. Heroin is self medication. It doesn't mean heroin causes mental health issues. Too many associations implying cause.

 

[markosheehan]

Also considering different benzodiazepines(different pharmacology subunits) have higher correlations with alzeimhers prooves benzodiazepines are the causing factor.

Other wise they would be no change in correlation when changing the benzodiazepines.

 

[Coolwhip]

I don't disagree with that take markosheehan, but the contrarian in me must point out that it isn't necessarily true. As different benzos are applied for different reasons, they aren't selected at random. Xanax is more likely to be employed for panic attacks, valium/temazepam for insomnia, clonazepam for GAD, more potent benzos will be prescribed for more severe symptoms, benzodiazepine utilization is even affected by geography, marketing, and patient request(resulting in different populations receiving different benzos).

 

[Limpet_Chicken]

Why the B12 nasal spray in auties? do you also use it for aspies? and are there any positive results shown after a while of the B12 supplementation? and if so, what?

I'm Kanner's myself, and wondering if you'd recommend trying it (although it'd have to be oral, I don't think I could access the nasal spray version, although I could always make one myself [and what form of B12 would you recommend using?) not that I'm looking to rid myself of my autistic traits, I'd fucking hate that, it would be no less than a nightmare made true, being autistic is fucking great

 

[mr peabody]

Study provides robust evidence of sex differences with Alzheimer’s gene

Summary: According to researchers, Alzheimer’s disease may be more prevalent in women, not simply because they live longer on average, but due to the APOE E4 gene. Researchers found the APOE association was greater for women in the Tau pathway than in men. However, there was no difference between APOE expression in the amyloid pathway in women compared to men.

The APOE gene, the strongest genetic risk factor for Alzheimer’s disease, may play a more prominent role in disease development among women than men, according to new research from the Vanderbilt Memory and Alzheimer’s Center.

The research confirmed recent studies that carrying the APOE ε4 allele has a greater association with Alzheimer’s disease among women compared to men, and went one step further by evaluating its association with amyloid and tau levels.

The study published May 7 in JAMA Neurology adds to mounting evidence that the higher prevalence of Alzheimer’s disease among women may not simply be a consequence of longer longevity. Almost two-thirds of Americans with Alzheimer’s are women. The research, based on a meta-analysis of both cerebral spinal fluid (CSF) samples from study volunteers from four datasets and autopsy findings from six datasets of Alzheimer-diseased brains, is the most robust evidence to date that the APOE gene may play a greater role in women than men in developing Alzheimer’s pathology, said Timothy J. Hohman, PhD, assistant professor of Neurology and the study’s lead author.

“In Alzheimer’s disease, we have not done enough to evaluate whether or not sex is a contributing factor to the neuropathology,” Hohman said. “We haven’t fully evaluated sex as a biological variable. But there is good reason to expect in older adulthood that there would be hormonal differences between the sexes that could impact disease.”

The study looked at whether APOE in men and women was primarily associated with the amyloid pathway — the proteins that form plaques in the brain — or with the tau pathway — the proteins that form tangles in the brain.

The association with the amyloid pathway was the same in men and women. However, the APOE association was much greater for women with the tau pathway. This is opposite of what researchers expected because of APOE’s established role in amyloid processing.

“The prevailing hypothesis of disease in Alzheimer’s is that amyloid comes online first and downstream is where we see tau changes that ultimately drive neurodegenerative changes,”
Hohman said.

Further analysis revealed that the sex difference with tau levels was present in amyloid-positive individuals — those with higher levels of amyloid plaque as determined by their CSF amyloid levels. The research suggests that APOE may modulate risk for neurodegeneration in a sex-specific manner, particularly in the presence of amyloidosis.

The study looked at whether APOE in men and women was primarily associated with the amyloid pathway —
the proteins that form plaques in the brain — or with the tau pathway —
the proteins that form tangles in the brain.

The greater association with tau occurred in CSF samples, but not with the autopsy datasets.

The reason for the contradiction between CSF samples and autopsy datasets could be because Braak staging — the method for quantifying the degree of tau tangle pathology at autopsy — measures a different aspect of tau pathology than what is measured in CSF.

“The way Braak staging works is you are actually looking at where in the cortex you see tangles at autopsy,” Hohman explained. “So it is not a measure of how many tangles are there. It is a measure of where those tangles are located.



Another possibility is that CSF tau may be an indicator of a more general neurodegenerative process that is not specific to tangle pathology.

“This study is at least moving toward bringing sex as a biological variable into our analyses and thinking about sex differences. Do we see differences in disease that could tell us something about the biology of the disease and could help both sexes in terms of coming up with treatment approaches? I think that the right treatment approach for a female above the age of 65 may end up being different than what it is for a male. Really the only way to find out is to look.”

http://neurosciencenews.com/apoe-sex-differences-9014/

 

[mr peabody]

Government’s top doctor 'tried to discredit claims Alzheimer's might be infectious'

A senior government adviser attempted to undermine a controversial study suggesting that Alzheimer’s is a transmissible disease before it was published in the journal Nature.

Dame Sally Davies, the chief medical officer at the Department of Health, approached the editor of a rival scientific journal, The Lancet, to discredit the study in the eyes of the public,
The Independent understands.

Dame Sally told Richard Horton, the editor of The Lancet, that the study on Alzheimer’s was likely to result in a public scare and asked him for advice on how to handle the media reaction before it came out in Nature.

The study, published earlier this month, suggested that the “seeds” of Alzheimer’s disease may be transmitted from one person to another during certain medical procedures.

It was based on the brain autopsies of eight people aged between 36 and 51 who had died of Creutzfeldt-Jakob disease (CJD) after receiving injections of human growth hormone derived from the pituitary glands of dead people.

Seven of the eight has signs of a brain protein linked with Alzheimer’s, although they had no genetic predisposition to the disease and were too young to have developed it naturally – strongly suggesting transmission via contaminated hormone injections.

Dame Sally, a haematologist by training, contacted Dr Horton on the weekend before Nature intended to publish the study having received confidential information under the strict embargo terms of the journal, which prohibit any approaches to third parties unless it is “solely for soliciting informed comment”.

In an unsigned editorial in The Lancet this week, Dr Horton writes that an unnamed government source informed him on the study’s impending publication and urged him to consider what he might do to reduce further the risk of a scare.

Dr Horton then wrote to the Science Media Centre in London, which was coordinating expert reaction to the study with the help of University College London and the Medical Research Council, which funded the work by Professor John Collinge, a world authority on transmissible brain diseases.

Although The Lancet’s source is not identified, The Independent understands that it was Dame Sally, who knows Dr Horton personally and has shared several conference platforms with The Lancet’s outspoken editor.

A spokesman for the Department of Health said last night that the identity of The Lancet’s source is the subject of a freedom of information request and cannot therefore comment.

It is highly unusual for a government science adviser to approach a medical journal for help in media management relating to a controversial study published in a rival journal with its own distinguished track-record of handling contentious research findings.

A spokeswoman for Nature declined to comment. Sir Philip Campbell, its editor, was unavailable for comment.

In The Lancet’s editorial “Alzheimergate? When miscommunication met sensationalism”, Dr Horton attempts to belittle the significance of the study’s findings and the resulting newspaper coverage, including that of The Independent whose headline “Alzheimer’s may be a transmissible infection” is one of several he singles out for criticism.

“But the study does not provide evidence of human transmission, as the authors acknowledge themselves in their final paragraph – ‘there is no suggestion that Alzheimer’s disease is a contagious disease and no supportive evidence from epidemiological studies that Alzheimer’s disease is transmissible’,” Dr Horton writes.

The phrase mirrors the comment by Dame Sally issued hours before the Nature study was published: “As this research itself states, there is no evidence that Alzheimer's disease can be transmitted in humans, nor is there any evidence that Alzheimer's disease can be transmitted through any medical procedure.”

The Independent’s coverage of the study made it clear that Alzheimer’s is not contagious and cannot be “caught” by living with or caring for a patient. However we stated that the findings suggest that the “seeds” of the disease may be transmissible under certain circumstances, such as the injection of human growth hormone made from pituitary glands, which was stopped in 1985.

We also quoted Professor Collinge, who said during a press conference prior to the study’s publication: “Although it is not cause for alarm that it is in any way contagious, it doesn’t mean we shouldn’t think about whether there might be accidental routes by which this disease might be transmitted by certain medical procedures.”

Dr Horton also criticises the headline of the Nature study, which suggested it was “evidence of human transmission” of one of the brain proteins found in Alzheimer’s patients, and the use by some media of the phrase “paradigm shift”, which was cited several times by Professor Collinge in various press conferences.

“But the findings, although certainly interesting, were a long way from a true ‘paradigm shift’. The use of this phrase likely heightened the interest and attention of journalists – and headline writers,” Dr Horton wrote.

Dr Horton was unavailable for comment.

https://www.independent.co.uk/news/...-alzheimers-might-be-infectious-10514671.html

 

[mr peabody]

Synthetic molecule appears to reverse Alzheimer's-related neurological damage

Under ordinary circumstances, the protein tau contributes to the normal, healthy functioning of brain neurons. In some people, though, it collects into toxic tangles that damage brain cells. Such tangles are a hallmark of Alzheimer's and other neurodegenerative diseases.

But researchers at Washington University School of Medicine in St. Louis have shown that levels of the tau protein can be reduced - and some of the neurological damage caused by tau even reversed ?- by a synthetic molecule that targets the genetic instructions for building tau before the protein is made.

The study, in mice and monkeys, is published Jan. 25 in Science Translational Medicine. The findings suggest that the molecule - known as an antisense oligonucleotide - potentially could treat neurodegenerative diseases characterized by abnormal tau, including Alzheimer's.

"We've shown that this molecule lowers levels of the tau protein, preventing and, in some cases, reversing the neurological damage," said Timothy Miller, MD, PhD, the David Clayson Professor of Neurology and the study's senior author. "This compound is the first that has been shown to reverse tau-related damage to the brain that also has the potential to be used as a therapeutic in people."

Miller, then-graduate student Sarah DeVos, PhD, and colleagues studied genetically modified mice that produce a mutant form of human tau that easily clumps together. These mice start showing tau tangles at around 6 months of age and exhibit some neuronal damage by 9 months.

To reduce tau, the researchers used an antisense oligonucleotide, a kind of molecule that interferes with the instructions for building proteins. Genes in the DNA are copied into RNA, a messenger molecule that carries the instructions for building a protein. Antisense oligonucleotides bind to the messenger RNA and target it for destruction before the protein can be built. Such oligonucleotides can be designed to target the RNA for almost any protein.

The researchers administered a dose of the anti-tau oligonucleotide to 9-month-old mice every day for a month and then measured the amount of tau RNA, total tau protein and tangles of tau protein in their brains when the mice were 12 months old. The levels of all three were significantly reduced in the treated mice compared with mice that received a placebo.

Importantly, levels of total tau and tau tangles in the brains of treated 12-month-old mice were lower than in untreated 9-month-old mice, suggesting that the treatment not only had stopped but reversed the buildup of tau.

By the time this strain of genetically modified mice reaches 9 months of age, the hippocampus - a part of the brain important for memory - typically is visibly shrunken and shows dying neurons. But with the oligonucleotide treatment, the shrinkage and cell death were halted. There was not, however, any evidence of reversal of neuronal death.

The treated mice lived an average of 36 days longer than untreated mice, and they were better at building nests, which reflects a combination of social behavior, cognitive performance and motor capabilities. All of these functions can be impaired in people with Alzheimer's disease and other tau-related neurodegenerative diseases.

Oligonucleotide treatments recently have been approved by the Food and Drug Administration for two neuromuscular diseases: Duchenne's muscular dystrophy and spinal muscular atrophy (SMA). The oligonucleotide for SMA was discovered by Ionis Pharmaceuticals, which partnered with Miller to develop the oligonucleotide treatment for tau-related neurological diseases. Washington University holds joint patent applications with Ionis Pharmaceuticals on the use of oligonucleotides for reducing tau levels.

Human trials of oligonucleotides for several other neurological diseases are underway, including Huntington's disease and amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrig's disease. Miller co-leads the ALS trial.

Miller and colleagues were intrigued by the possibility of designing studies to lower tau in people, but first they needed to see how the oligonucleotide worked in an animal more similar to people than a mouse.

The researchers treated groups of healthy cynomolgus monkeys - also known as crab-eating macaques - with two doses of placebo or oligonucleotide, one week apart, directly into the cerebrospinal fluid that surrounds the spinal cord and brain, just as would be done with human patients. Two weeks later, they measured the amount of tau protein and RNA in the monkeys' brains and cerebrospinal fluid.

The oligonucleotide reduced both tau RNA and protein in the brain, and this reduction was mirrored in the cerebrospinal fluid.

"The monkey study showed us that lower tau in the cerebrospinal fluid correlates with lower tau in the brain," Miller said. "This is important if we're going to evaluate this treatment approach in people, because there's no non-invasive way of measuring tau levels in the brain. This correlation tells us that we can use levels of tau in the cerebrospinal fluid as a proxy for levels of tau in the brain."

Tau tangles are associated not just with Alzheimer's but with a range of lesser-known neurodegenerative diseases, such as progressive supranuclear palsy and corticobasal ganglionic degeneration. Tau levels also increase in the aftermath of traumatic brain injury, which can lead to dementia.

"Tau tangles correlate with cognitive decline in several diseases," Miller said. "This is a promising new approach to lowering tau, but we have to test whether it is safe in people, and whether it actually lowers tau, as it is designed to do, before we get to the question of whether it has any effect on the disease. But everything we've seen so far says that this is worth investigating as a potential treatment for people."

https://www.news-medical.net/news/2...e-Alzheimers-related-neurological-damage.aspx

 

[Limpet_Chicken]

Whether or not its safe? I imagine there would be an awful lot of people diagnosed with the very beginning stages of alzheimer's who'd say 'fuck the animal testing, use me as your guinea pig'.

As far as daily dosing of the antisense oligo goes, wonder how well incorporating the antisense coding sequence into a replication-incompetent retroviral vector would work? potentially removing the need for frequent dosing, having the body produce the antitau sequence in-situ.

Pretty fucking disgusting that some slimy greaseball in govt. tried to step in and fuck with the publication of a medical (or any other) scientific journal article though...damn! quite what the flying fuck do the likes of health advisors actually know about medicine itself? they might understand how to manage (well, sort of) a health system at the national level, but they have no business whatsoever getting involved with the sharp end of medical procedure, or with medical science, that just isn't where their competency, if I can debase the word in using it to relate to a politician, lies.

Although why does it not surprise me one bloody bit. Disgusts me alright, but surprised? am I hell, afterall, you can't very well expect to keep a nest of vipers without having the poison along with it.

 

[AlphaMethylPhenyl]

The most natural and healthful manner of battling any possible looming dementia in the future is to work your brain. I believe crossword puzzles have a great amount of utility in this respect, as it was found. Coffee in moderation seems beneficial.

Herbs such as ashwagandha (sp?) and particularly tulsi (holy basil) are adaptogens. They are thought to help restore the body to a healthy homeostasis. Tulsi is known for healing damage to the adrenal gland. I found peace and focus in it.

Polluting your body with all these strong psychoactives isn't going to work. I don't think you're going to piece together a pharmacological magic bullet to battle any sort of neurodegeneration. Better is developing positive habits.