White matter abnormalities in long-term AAS users

A

alan2102

Greenlighter
Joined
Dec 30, 2016
Messages
42

https://www.ncbi.nlm.nih.gov/pubmed/27988413

Psychiatry Res. 2017 Feb 28;260:1-5. doi: 10.1016/j.pscychresns.2016.12.003. Epub 2016 Dec 10.

White matter abnormalities in long-term anabolic-androgenic steroid users: A pilot study.

Seitz J1, Lyall AE2, Kanayama G3, Makris N4, Hudson JI3, Kubicki M4, Pope HG Jr3, Kaufman MJ5.

Abstract

Recent studies of long-term anabolic-androgenic steroid (AAS) users reported amygdala structural and functional connectivity abnormalities. We assessed white matter microstructure in the inferior-fronto-occipital fasciculus (IFOF), a major associative bundle of the amygdala network. Diffusion weighted images acquired from 9 male long-term AAS users and 8 matched controls aged 36-51 years old were processed using a standardized pipeline (Tract-Based Spatial Statistics). Group differences were examined using linear regression with adjustment for age and current testosterone level. Compared to nonusers, AAS users exhibited significantly higher fractional anisotropy (FA) in the IFOF. Users showed markedly greater FA than nonusers on the left IFOF but only a modest, nonsignificant difference on the right IFOF. Moreover, FA was positively associated with lifetime cumulative AAS dose. Our results suggest that long-term AAS use alters IFOF white matter organization and integrity, which in turn might affect amygdala-related processes such as reward system function. Accordingly, further studies are needed to replicate findings in larger subject groups to determine the functional significance of the FA abnormality.

Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.


KEYWORDS:

(4): Diffusion tensor imaging (DTI); Anabolic-androgenic steroids (AAS); Inferior-fronto-occipital fasciculus (IFOF); Tract-based spatial statistics (TBSS)

PMID:27988413PMCID:PMC5272808 [Available on 2018-02-28]DOI:
10.1016/j.pscychresns.2016.12.003
 
Interesting, thanks for posting. There've been a few studies demonstrating abnormalities now. We really need to see what functional difference this makes. Fingers crossed they'll be following this up.
 
Great, we're fucking up our brains boyos...



Kidding, but more research needs to be done. I'm assuming this would be more so tren related?
 
Intense said:
Great, we're fucking up our brains boyos...
Click to expand...

There's use, and overuse, and abuse. Different things.

This just came to my attention, and it has interesting implications for cognition, mood, and other stuff. Perhaps MODEST activation of the androgen receptor (with androgens, or perhaps SARMS) can upregulate myelin repair, and hence have a salutary effect on a number of conditions.

....................................

Proc Natl Acad Sci U S A. 2016 Dec 20;113(51):14829-14834. doi: 10.1073/pnas.1614826113. Epub 2016 Dec 7.

Unexpected central role of the androgen receptor in the spontaneous regeneration of myelin.

Bielecki B1,2, Mattern C3, Ghoumari AM1, Javaid S1,4, Smietanka K1,2, Abi Ghanem C1, Mhaouty-Kodja S5, Ghandour MS6,7, Baulieu EE8, Franklin RJ9,10, Schumacher M8, Traiffort E1.

Author information


Abstract

Lost myelin can be replaced after injury or during demyelinating diseases in a regenerative process called remyelination. In the central nervous system (CNS), the myelin sheaths, which protect axons and allow the fast propagation of electrical impulses, are produced by oligodendrocytes. The abundance and widespread distribution of oligodendrocyte progenitors (OPs) within the adult CNS account for this remarkable regenerative potential. Here, we report a key role for the male gonad, testosterone, and androgen receptor (AR) in CNS remyelination. After lysolecithin-induced demyelination of the male mouse ventral spinal cord white matter, the recruitment of glial fibrillary acidic protein-expressing astrocytes was compromised in the absence of testes and testosterone signaling via AR. Concomitantly, the differentiation of OPs into oligodendrocytes forming myelin basic protein (MBP)+ and proteolipid protein-positive myelin was impaired. Instead, in the absence of astrocytes, axons were remyelinated by protein zero (P0)+ and peripheral myelin protein 22-kDa (PMP22)+ myelin, normally only produced by Schwann cells in the peripheral nervous system. Thus, testosterone favors astrocyte recruitment and spontaneous oligodendrocyte-mediated remyelination. This finding may have important implications for demyelinating diseases, psychiatric disorders, and cognitive aging. The testosterone dependency of CNS oligodendrocyte remyelination may have roots in the evolutionary history of the AR, because the receptor has evolved from an ancestral 3-ketosteroid receptor through gene duplication at the time when myelin appeared in jawed vertebrates.

KEYWORDS:

Schwann cells; androgen receptor; myelin; oligodendrocytes; testosterone

PMID:27930320PMCID:PMC5187716 [Available on 2017-06-20]DOI:10.1073/pnas.1614826113
 
alan2102 said:
There's use, and overuse, and abuse. Different things.

This just came to my attention, and it has interesting implications for cognition, mood, and other stuff. Perhaps MODEST activation of the androgen receptor (with androgens, or perhaps SARMS) can upregulate myelin repair, and hence have a salutary effect on a number of conditions.

....................................

Proc Natl Acad Sci U S A. 2016 Dec 20;113(51):14829-14834. doi: 10.1073/pnas.1614826113. Epub 2016 Dec 7.

Unexpected central role of the androgen receptor in the spontaneous regeneration of myelin.

Bielecki B1,2, Mattern C3, Ghoumari AM1, Javaid S1,4, Smietanka K1,2, Abi Ghanem C1, Mhaouty-Kodja S5, Ghandour MS6,7, Baulieu EE8, Franklin RJ9,10, Schumacher M8, Traiffort E1.

Author information


Abstract

Lost myelin can be replaced after injury or during demyelinating diseases in a regenerative process called remyelination. In the central nervous system (CNS), the myelin sheaths, which protect axons and allow the fast propagation of electrical impulses, are produced by oligodendrocytes. The abundance and widespread distribution of oligodendrocyte progenitors (OPs) within the adult CNS account for this remarkable regenerative potential. Here, we report a key role for the male gonad, testosterone, and androgen receptor (AR) in CNS remyelination. After lysolecithin-induced demyelination of the male mouse ventral spinal cord white matter, the recruitment of glial fibrillary acidic protein-expressing astrocytes was compromised in the absence of testes and testosterone signaling via AR. Concomitantly, the differentiation of OPs into oligodendrocytes forming myelin basic protein (MBP)+ and proteolipid protein-positive myelin was impaired. Instead, in the absence of astrocytes, axons were remyelinated by protein zero (P0)+ and peripheral myelin protein 22-kDa (PMP22)+ myelin, normally only produced by Schwann cells in the peripheral nervous system. Thus, testosterone favors astrocyte recruitment and spontaneous oligodendrocyte-mediated remyelination. This finding may have important implications for demyelinating diseases, psychiatric disorders, and cognitive aging. The testosterone dependency of CNS oligodendrocyte remyelination may have roots in the evolutionary history of the AR, because the receptor has evolved from an ancestral 3-ketosteroid receptor through gene duplication at the time when myelin appeared in jawed vertebrates.

KEYWORDS:

Schwann cells; androgen receptor; myelin; oligodendrocytes; testosterone

PMID:27930320PMCID:PMC5187716 [Available on 2017-06-20]DOI:10.1073/pnas.1614826113
Click to expand...



Thanks for this alan. I'm going to tack it on to our other thread on the subject >>here<< as it's a directly relevant follow-on, and further evidence of the potential benefit of AAS.
 
You must log in or register to reply here.
Top