New Alzheimer's treatments may arise from modeling 'heat shock proteins'

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Tincup
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New Alzheimer's treatments may arise from modeling 'heat shock proteins'

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Thanks to Rhonda Patrick:
One of the hallmarks of Alzheimer's disease is the abnormal clumping of beta-amyloid proteins in the brain, resulting in the death of brain cells. The discovery that small heat shock proteins prevent uncontrolled protein clumping has opened the possibility of developing drugs that emulate this effect. Now, a new study takes this a step further by revealing how small heat shock proteins interact with beta-amyloid to prevent clumping.
http://www.medicalnewstoday.com/articles/300878.php

Rhonda talks about creating heat shock proteins using saunas. Interesting...

Her blog: https://foundmyfitness.com/ iTunes: https://itunes.apple.com/us/podcast/fou ... 98322?mt=2
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Re: New Alzheimer's treatments may arise from modeling 'heat shock proteins'

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It looks like exercise can also affect heat shock proteins in human brains in vivo:
Full text: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065286/
Exercise induces the release of heat shock protein 72 from the human brain in vivo
G. I. Lancaster,1 K. Møller,2 B. Nielsen,3 N. H. Secher,4 M. A. Febbraio,1 and L. Nybo3
Author information ► Article notes ► Copyright and License information ►
This article has been cited by other articles in PMC.
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Abstract

The present study tested the hypothesis that in response to physical stress the human brain has the capacity to release heat shock protein 72 (Hsp72) in vivo. Therefore, 6 humans (males) cycled for 180 minutes at 60% of their maximal oxygen uptake, and the cerebral Hsp72 response was determined on the basis of the internal jugular venous to arterial difference and global cerebral blood flow. At rest, there was a net balance of Hsp72 across the brain, but after 180 minutes of exercise, we were able to detect the release of Hsp72 from the brain (335 ± 182 ng/min). However, large individual differences were observed as 3 of the 6 subjects had a marked increase in the release of Hsp72, whereas exercise had little effect on the cerebral Hsp72 balance in the remaining 3 subjects. Given that cerebral blood flow was unchanged during exercise compared with values obtained at rest, it is unlikely that the cerebral Hsp72 release relates to necrosis of specific cells within the brain. These data demonstrate that the human brain is able to release Hsp72 in vivo in response to a physical stressor such as exercise. Further study is required to determine the biological significance of these observations.
There are a lot of heat shock proteins of which I basically know nothing, but maybe this is part of the benefit of exercise on the aging brain.
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Re: New Alzheimer's treatments may arise from modeling 'heat shock proteins'

Post by Kathleen1 »

In any case, the heat shock protein articles lets me luxuriate in the sauna. Like coffee, chocolate, music---so many good things good for you. Please now tell me that the sauna provides me with the same benefits as exercise.
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Re: New Alzheimer's treatments may arise from modeling 'heat shock proteins'

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Richard, do you think if we exercise well over the 60% max (i.e. 80% for 40 minutes), produce the HSP benefits earlier than "180 minutes of exercise"? Am I correctly reading 3 hours of exercise at 60%max?
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Re: New Alzheimer's treatments may arise from modeling 'heat shock proteins'

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Kitano wrote:Richard, do you think if we exercise well over the 60% max (i.e. 80% for 40 minutes), produce the HSP benefits earlier than "180 minutes of exercise"? Am I correctly reading 3 hours of exercise at 60%max?
I'm viewing this as a proof of concept piece rather than a source of guidance about the intensity of exercise needed.
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Re: New Alzheimer's treatments may arise from modeling 'heat shock proteins'

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More interesting findings on heat shock proteins. Here's the summary.
The endoplasmic reticulum (ER) is a membrane structure found in mammalian cells. It carries out a number of important functions, including the synthesis, folding, modification and transport of proteins needed on the surface or outside the cell. Dr Avezov and colleagues hypothesised that stressing the ER might lead to protein misfolding and aggregation by diminishing its ability to function correctly, leading to increased aggregation.

They were surprised to discover the opposite was true.

"We were astonished to find that stressing the cell actually eliminated the aggregates -- not by degrading them or clearing them out, but by unravelling the aggregates, potentially allowing them to refold correctly," said Dr Avezov.

"If we can find a way of awakening this mechanism without stressing the cells -- which could cause more damage than good -- then we might be able to find a way of treating some dementias."

The main component of this mechanism appears to be one of a class of proteins known as heat shock proteins (HSPs), more of which are made when cells are exposed to temperatures above their normal growth temperature, and in response to stress.

Dr Avezov speculates that this might help explain one of the more unusual observations within the field of dementia research. "There have been some studies recently of people in Scandinavian countries who regularly use saunas, suggesting that they may be at lower risk of developing dementia. One possible explanation for this is that this mild stress triggers a higher activity of HSPs, helping correct tangled proteins."
https://www.sciencedaily.com/releases/2 ... 102618.htm


Stress-induced protein disaggregation in the endoplasmic reticulum catalysed by BiP. Nature Communications, 2022; 13 (1) DOI: 10.1038/s41467-022-30238-2
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