ALZHEIMER'S | +80 articles

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Cranberries significantly improved the participants’ memory of everyday events
(visual episodic memory), neural functioning and delivery of blood to the brain.

Cranberries found to improve memory, ward off Dementia*

University of East Anglia | Neuroscience News | 30 May 2022

Older adults who consumed cranberries frequently as part of their diet saw improvements in episodic memory, neural function, and brain perfusion. Cranberry consumption was also linked to a significant decrease in LDL cholesterol. Findings reveal adding cranberries to the diet helps to improve memory and could protect against dementia.

Adding cranberries to your diet could help improve memory and brain function, and lower ‘bad’ cholesterol – according to new research from the University of East Anglia (UK).

A new study published today highlights the neuroprotective potential of cranberries.

The research team studied the benefits of consuming the equivalent of a cup of cranberries a day among 50 to 80-year-olds.

They hope that their findings could have implications for the prevention of neurodegenerative diseases such as dementia.

Lead researcher Dr David Vauzour, from UEA’s Norwich Medical School, said: “Dementia is expected to affect around 152 million people by 2050. There is no known cure, so it is crucial that we seek modifiable lifestyle interventions, such as diet, that could help lessen disease risk and burden."

“Past studies have shown that higher dietary flavonoid intake is associated with slower rates of cognitive decline and dementia. And foods rich in anthocyanins and proanthocyanidins, which give berries their red, blue, or purple colour, have been found to improve cognition."

“Cranberries are rich in these micronutrients and have been recognized for their antioxidant and anti-inflammatory properties."

“We wanted to find out more about how cranberries could help reduce age-related neurodegeneration.”

The research team investigated the impact of eating cranberries for 12 weeks on brain function and cholesterol among 60 cognitively healthy participants.

Half of the participants consumed freeze-dried cranberry powder, equivalent to a cup or 100g of fresh cranberries, daily. The other half consumed a placebo.

The study is one of the first to examine cranberries and their long-term impact on cognition and brain health in humans.

The results showed that consuming cranberries significantly improved the participants’ memory of everyday events (visual episodic memory), neural functioning and delivery of blood to the brain (brain perfusion).

Dr Vauzour said: “We found that the participants who consumed the cranberry powder showed significantly improved episodic memory performance in combination with improved circulation of essential nutrients such as oxygen and glucose to important parts of the brain that support cognition – specifically memory consolidation and retrieval."

“The cranberry group also exhibited a significant decrease in LDL or ‘bad’ cholesterol levels, known to contribute to atherosclerosis – the thickening or hardening of the arteries caused by a build-up of plaque in the inner lining of an artery. This supports the idea that cranberries can improve vascular health and may in part contribute to the improvement in brain perfusion and cognition."

“Demonstrating in humans that cranberry supplementation can improve cognitive performance and identifying some of the mechanisms responsible is an important step for this research field."

“The findings of this study are very encouraging, especially considering that a relatively short 12-week cranberry intervention was able to produce significant improvements in memory and neural function,” he added.

“This establishes an important foundation for future research in the area of cranberries and neurological health.

Original Research: Open access.
“Chronic consumption of Cranberries (Vaccinium macrocarpon) for 12 weeks improves episodic memory and regional brain perfusion in healthy older adults: A randomised, placebo-controlled, parallel-groups study” by David Vauzour et al. Frontiers in Nutrition​

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Abstract

Chronic consumption of Cranberries (Vaccinium macrocarpon) for 12 weeks improves episodic memory and regional brain perfusion in healthy older adults: A randomised, placebo-controlled, parallel-groups study

Background: Ageing is highly associated with cognitive decline and modifiable risk factors such as diet are believed to protect against this process. Specific dietary components and in particular, (poly)phenol-rich fruits such as berries have been increasingly recognised for their protection against age-related neurodegeneration. However, the impact of cranberries on cognitive function and neural functioning in older adults remains unclear.

Design: A 12-week parallel randomised placebo-controlled trial of freeze-dried cranberry powder was conducted in 60 older adults aged between 50 and 80 years. Cognitive assessment, including memory and executive function, neuroimaging and blood sample collection were conducted before and after the intervention to assess the impact of daily cranberry consumption on cognition, brain function and biomarkers of neuronal signalling.

Results: Cranberry supplementation for 12 weeks was associated with improvements in visual episodic memory in aged participants when compared to placebo. Mechanisms of action may include increased regional perfusion in the right entorhinal cortex, the accumbens area and the caudate in the cranberry group. Significant decrease in low-density lipoprotein (LDL) cholesterol during the course of the intervention was also observed. No significant differences were, however, detected for BDNF levels between groups.

Conclusions: The results of this study indicate that daily cranberry supplementation (equivalent to 1 small cup of cranberries) over a 12-week period improves episodic memory performance and neural functioning, providing a basis for future investigations to determine efficacy in the context of neurological disease.

*From the article here :

How Cranberries Could Improve Memory and Ward off Dementia - Neuroscience News

Older adults who consumed cranberries frequently as part of their diet saw improvements in episodic memory, neural function, and brain perfusion. Cranberry consumption was also linked to a significant decrease in LDL cholesterol. Findings reveal adding cranberries to the diet helps to improve...

neurosciencenews.com

I buy big bags of Ocean Spray Craisins (dried cranberries) from Costco and eat them every day in cereal or granola. Fantastic! - PB​

 

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Alzheimer’s Disease causes cells to overheat and ‘fry like eggs’​

University of Cambridge | Neueoscience News

Researchers have shown that aggregation of amyloid-beta, one of two key proteins implicated in Alzheimer’s disease, causes cells to overheat and ‘fry like eggs.’

The researchers, from the University of Cambridge, used sensors small and sensitive enough to detect temperature changes inside individual cells, and found that as amyloid-beta misfolds and clumps together, it causes cells to overheat.

In an experiment using human cell lines, the researchers found the heat released by amyloid-beta aggregation could potentially cause other, healthy amyloid-beta to aggregate, causing more and more aggregates to form.

In the same series of experiments, the researchers also showed that amyloid-beta aggregation can be stopped, and the cell temperature lowered, with the addition of a drug compound. The experiments also suggest that the compound has potential as a therapeutic for Alzheimer’s disease, although extensive tests and clinical trials would first be required.

The researchers say their assay could be used as a diagnostic tool for Alzheimer’s disease, or to screen potential drug candidates.

The results are reported in the Journal of the American Chemical Society.

Alzheimer’s disease affects an estimated 44 million people worldwide, and there are currently no effective diagnostics or treatments. In Alzheimer’s disease, amyloid-beta and another protein called tau build up into tangles and plaques – known collectively as aggregates – causing brain cells to die and the brain to shrink. This results in memory loss, personality changes and difficulty carrying out daily functions.

It is a difficult disease to study, since it develops over decades, and a definitive diagnosis can only be given after examining samples of brain tissue after death. It is still not known what kind of biochemical changes inside a cell lead to amyloid-beta aggregation.

In Professor Gabriele Kaminski Schierle’s research group at Cambridge’s Department of Chemical Engineering and Biotechnology, they have been investigating the possible link between temperature and amyloid-beta aggregation in human cells.

The field of studying temperature changes inside a cell is known as intracellular thermogenesis. It is a new and challenging field: scientists have developed sensors with which temperature changes can be measured, however, no one has ever tried to use these sensors to study conditions such as Alzheimer’s disease.

“Thermogenesis has been associated with cellular stress, which may promote further aggregation,” said Chyi Wei Chung, the study’s first author. “We believe that when there’s an imbalance in cells, like when the amyloid-beta concentration is slightly too high and it starts to accumulate, cellular temperatures increase.”

“Overheating a cell is like frying an egg – as it heats up, the proteins start to clump together and become non-functional,” said Kaminski Schierle, who led the research.

The researchers used tiny temperature sensors called fluorescent polymeric thermometers (FTPs) to study the link between aggregation and temperature. They added amyloid-beta to human cell lines to kickstart the aggregation process and used a chemical called FCCP as a control, since it is known to induce an increase in temperature.

They found that as amyloid-beta started to form thread-like aggregates called fibrils, the average temperature of the cells started to rise. The increase in cellular temperature was significant compared to cells that did not have any amyloid-beta added.

“As the fibrils start elongating, they release energy in the form of heat,” said Kaminski Schierle. “Amyloid-beta aggregation requires quite a lot of energy to get going, but once the aggregation process starts, it speeds up and releases more heat, allowing more aggregates to form.”

“Once the aggregates have formed, they can exit the cell and be taken up by neighbouring cells, infecting healthy amyloid-beta in those cells,” said Chung. “No one has shown this link between temperature and aggregation in live cells before.”

Using a drug that inhibits amyloid-beta aggregation, the researchers were able to pinpoint the fibrils as the cause of thermogenesis. It had previously been unknown whether protein aggregation or potential damage to mitochondria – the ‘batteries’ that power cells – was responsible for this phenomenon.

The researchers also found that the rise in cellular temperatures could be mitigated by treating them with an aggregation inhibitor, highlighting its potential as a therapeutic for Alzheimer’s disease.

The laboratory experiments were complemented by computational modelling describing what might happen to amyloid-beta in an intracellular environment and why it might lead to an increase in intracellular temperatures. The researchers hope their work will motivate new studies incorporating different parameters of physiological relevance.

Author: Sarah Collins
Source: University of Cambridge
Contact: Sarah Collins – University of Cambridge
Image: The image is credited to Chyi Wei Chung

Original Research: Open access.
“Intracellular Aβ42 Aggregation Leads to Cellular Thermogenesis” by Chyi Wei Chung et al. Journal of the American Chemical Association

Alzheimer’s Disease Causes Cells to Overheat and ‘Fry Like Eggs’ - Neuroscience News

The heat produced by amyloid-beta aggregation may cause other, healthy amyloid-beta to aggregate, causing more and more aggregates to form. However, with the addition of a novel drug compound, amyloid-beta aggregation can be stopped and the cell temperature lowered.

neurosciencenews.com

 

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Cannabis may prevent the onset of Alzheimer's

by Steve Elliott

Early use of cannabis apparently delays and might even prevent the onset of Alzheimer's, according to a leading scientist in the field. But the work of longtime researcher Gary Wenk of Ohio State University has come to a halt, despite the promising results.

"We found out that people who smoked cannabis in the 1960s were not getting Alzheimer's," Wenk explained, reports KJ Hiramoto at the Seattle PI. "These 90-year-olds without dementia were telling us things like, 'Well, I drank whiskey and smoked cannabis,' and these are the things they remember. They don't remember habits like how often they ate broccoli."

Maddeningly, Wenk's research ground to a halt due to political, legal and financial reasons.

"The evidence in animals is clear but making the leap to humans means that you have to find a drug company willing to handle the lawsuits and the money," Wenk said.

He faced other hurdles, as well. Scientists who wish to research cannabis have to compete for approval and grants from the National Institute on Drug Abuse (NIDA), for which The University of Mississippi is the only source of cannabis - Mississppi has the only federally legal, grant-funded cannabis garden in the U.S.A.

What makes the situation even worse is that, as admitted even by NIDA Director Nora D. Valkow, M.D., is that the agency is only interested in studying the potential harms of cannabis, not the medicinal benefits.

A spokesperson for the NIDA told the New York Times in 2010 that the agency does not fund research focused on the potential medical benefits of cannabis.

"As the National Institute on Drug Abuse, our focus is primarily on the negative consequences of cannabis use," NIDA spokeswoman Shirley Simson told the Times.

And under federal law, the NIDA must approve all clinical research involving cannabis. It tightly controls which investigators are allowed access to the federal government's Ole Miss cannabis supply, which is grown (and then stored, for years) at the research facility in Oxford, Mississippi.

"I am not funded to do cannabis research," Wenk said. "It cost me about $100,000 to do a whole experiment, $10,000 just to buy the molecule, and every old rat is $150. You can see how it adds up, and individuals can't afford it."

British researchers find corroborating evidence

"A paper published in the British Journal of Pharmacology suggests that the cannabinoids in cannabis are likely not only to prevent the onset of Alzheimer's, but also of Parkinson's disease, Huntington's disease, and age-related dementia," reports Brandon Isaak.

Chronic brain inflammation, oxidative stress, and intra-cellular dysfunction are the primary reasons people develop these debilitating neurological diseases, and the study found that both THC and CBD, found in cannabis, help protect nerve cell function in users, significant reducing these harmful conditions.

The cannabinoids tap into the endocannabinoid system, reducing inflammation, protecting brain cells from oxidative damage, and promoting cellular health on multiple levels, according to the researchers.

Showing promise: Old people are going to win

Wenk's research, before it was halted, anyway, was showing promise to middle-aged and older Americans. Cannabinoids found in cannabis may delay the onset of Alzheimer's so effectively that people are more likely to die of old age before showing any signs of dementia.

In the study, Wenk dosed rats in his lab at Ohio State a dosage equivalent to one puff of cannabis every day. In old rats with impaired memory due to brain inflammation, that single puff a day was making them smarter. Not only were they more intelligent, but some of the pathological changes in the rats brains, due to aging, were being reversed.

"Essentially, what we found was that we know that as people get older, their neurogenesis drops to zero," Wenk said, referring to the process through which new brain cells are created. "And that's part of the reason old people have a problem with their memory and depression. What we found was that not only did the single puff a day reverse the memory impairment but also restarted neurogenesis."

According to Wenk, delaying the end of neurogenesis (regeneration of neurons) helps middle-aged Americans and their families in a very easy-to-measure way: in their pocketbooks.

"If we can keep a person out of a nursing home for five years, we've saved that family and their insurance companies an awful lot of money," Wenk said. "No matter how we spin this, old people are going to win."

"I am incredibly excited about it, because this is the first time we have ever had a compound that actually works in the old brain," Wenk said. "Everything works in the young brain, but this is working in old brains. So this means if you are, 60, 70, and you are having problems with mental decline? We might have a mechanism that could target that."

"Very low doses are effective," Wenk said, "Even just one puff of cannabis a day helps," according to his research. "This is just the beginning of what we believe we will uncover as we investigate this line of research," he said.

Blocking endocannabinoids may trigger early Alzheimers

Another study from a team of investigators at the Stanford University School of Medicine led by Daniel Madison has implicated the blocking of endocannabinoids, the brains own internal versions of the active compounds in cannabis, in the early pathology of Alzheimers.

It seems a substance called A-beta, suspected to play a key role in Alzheimers because it is the main part of clumps which dot the brains of Alzheimer's patients, may, in the early stages of the disease, impair learning and memory by blocking the beneficial action of endocannabinoids.

The group at Stanford is now trying to suss out the molecular details of how this occurs. Pinning down the details could pave the path to new ways to stave off the learning disabilities and memory deficits that characterize Alzheimer's and could also help explain how smoking cannabis helps to delay or even prevent its onset.

In the study, published in the June 28, 2014 issue of the scientific journal Neuron, the researchers detail how pyramidal cells in the brain underpin learning and memory. This assures, they learned, that high-intensity input such as falling down or burning your finger tends to stick in your memory, thus presumably help avoid such mishaps in the future.

Pyramidal cells are encouraged to ignore noise signals, they constantly receive random signals from upstream nerve cells by a sort of wet blanket, nerve cells called interneurons. These secret an inhibitory substance, the molecular equivalent of an indifferent shrug or yawn, signaling that the input is not really very important.

But when the news actually is significant, pyramidal cells secrete their own "Now just you wait a minute, these are important" chemicals. And guess what? Those chemicals which signal the importance of incoming information are none other than the endocannabinoids.

Madison speculates that when we smoke cannabis, the phytocannabinoids from the plant have the effect of enhancing the perceived importance of events that happen while we are under the influence of cannabis.

And another likely effect is inhibiting the "wet blanket effect" of interneurons which, in Alzheimers, needs reducing to increase the ability to learn and remember.

Increasing tolerance

The federal Schedule I illegality of cannabis, under which it is officially considered to have no medical uses and a high danger of abuse, has stymied Wenk's research. But the scientist has noticed a refreshing trend, a major shift in the cultural tolerance of cannabis, particularly from young people, including his students.

"I've really seen a shift in 10 years of increased cannabis tolerance," Wenk said. "In my class, people are more than willing to discuss their cannabis use. But they would be embarrassed to mention that they smoke cigarettes."

With Alzheimer's ranking as the sixth leading cause of death in the United States, and with more than five million Americans currently struggling with the disease, which has no known cure, you would think that lab results as promising as Wenk's would have attracted major funding by now. But that is not the case, because, as we have pointed out, the NIDA is not really interested in knowing about the medical benefits of cannabis, just its dangers.
Wenk, who has researched the effects of Alzheimer's on animals for about 40 years, has shared his findings in his book, Your Brain On Food.

https://tokesignals.com/marijuana-sh...ch-is-stalled/

 

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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.”

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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​