Comments for Guarente Lab Blog

Comment on Alzheimer’s by Eric

Eric — Sat, 15 Nov 2008 01:01:57 +0000

These two studies bring Abeta back it the Alzheimer’s disease discussion.

http://www.signaling-gateway.org/update/updates/200811/nrn2522.html

Comment on Alzheimer’s by cause of alzheimers disease

cause of alzheimers disease — Mon, 27 Oct 2008 09:01:44 +0000

cause of alzheimers disease…

There are others that think just like you. Good job….

Comment on Alzheimer’s by Hiram

Hiram — Sun, 05 Oct 2008 05:27:10 +0000

Hiram…

Dream as if you’ll live forever, live as if you’ll die today….

Comment on Alzheimer’s by JohnNOsa

JohnNOsa — Mon, 01 Sep 2008 18:59:22 +0000

very good

Comment on Alzheimer’s by admin

admin — Wed, 06 Aug 2008 13:43:41 +0000

Finally read through the article. I think guys you should make sure that you grasped the experimental design and therefore conclusions that can or can-not be made from it. And obviously it was not done.
(By the way, if you are interested in a course of how to read primary scientific literature, I am teaching one this Fall. :-) )

Immunization started before severe dementia started, therefore no one asks to repair existing damage. The hope was that removal of plaques would slow down further degeneration of neurons, which clearly did not happen (as judged by dementia levels of survival). So yes, of course plaques could already damaged neurons when vaccine was injected, but damage should have slowed down or being prevented when plaques were removed and dementia should have stayed level, not increase progressively.

Here is finding and conclusions from the paper:
Findings
20 participants—15 in the AN1792 group, five in the placebo group—died before follow-up started. A further 22 patients—19 in the AN1792 group, three in the placebo group—died during follow-up. Nine of the deceased patients, all in the AN1792 group, had given consent for post-mortem analysis; one of these who did not die with Alzheimer’s disease was excluded. In the remaining eight participants who received immunisation and who were examined neuropathologically, mean Aβ load was lower than in an unimmunised control group that was matched for age at death (2•1% [SE 0•7] in treated participants vs 5•1% [0•9] in controls; mean difference 3•0%, 95% CI 0•6–5•4; p=0•02). Although there was considerable variation in Aβ load and degree of plaque removal among immunised participants, the degree of plaque removal varied significantly with mean antibody response attained during the treatment study period (Kruskal-Wallis p=0•02). Seven of the eight immunised patients who underwent post-mortem assessment, including those with virtually complete plaque removal, had severe end stage dementia before death. In the whole cohort, there was no evidence of improved survival (hazard ratio 0•93, 95% CI 0•43–3•11; p=0•86) or of an improvement in the time to severe dementia (1•18, 0•45–3•11; p=0•73) in the AN1792 group versus the placebo group.

Interpretation
Although immunisation with Aβ42 resulted in clearance of amyloid plaques in patients with Alzheimer’s disease, this clearance did not prevent progressive neurodegeneration

Comment on Alzheimer’s by michael bonkowski

michael bonkowski — Wed, 06 Aug 2008 01:55:52 +0000

I’m with Kayvan on this! This finding only suggests that a reduction of absolute plaques accumulation does not prolong life or reduce measured outcomes of disease progression or reversal. For example, if these amyloid tangles are either causing neuronal dysfunction or a side effect of of neuronal damage, then a drug that reduces existing plaques would not neccesarily lead to heightened neuronal regeneration and plasticity. So while the stocks for this drug don’t rise, this finding provides further support for the MGH study released earlier this year in mice that suggested the behavioral symptoms precede the accumulation of plaques.

Comment on Alzheimer’s by libert

libert — Sat, 19 Jul 2008 00:36:52 +0000

As I understand cognitive functions deteriorate progressively over 4-6 years. Assuming plaques stopped accumulating and even dissolved over that period of time, suggests that they have little to do with dementia – real problem in this disease. This notion is not new. Several years ago a paper was published, which showed that amount of plaques has absolutely no correlation with dementia severity – yet “plaquers” just would not let go. They claimed that people are to genetically different, which is true. I think together with this paper and the fact that Alzheimer’s mice have lots of plaques and no obvious neurological phenotypes should finally concentrate research on the real problem.

Comment on Alzheimer’s by Kayvan

Kayvan — Sat, 19 Jul 2008 00:23:39 +0000

Very interesting… perhaps the patients were past the point of no return, so that even getting rid of the plaques still doesn’t help - the plaques have already reaped their damage. shouldnt they be using this in animal models???

Comment on Welcome to the Guarente Web Blog! by Kayvan

Kayvan — Fri, 18 Jul 2008 16:33:08 +0000

i second that.

Comment on Welcome to the Guarente Web Blog! by Serg

Serg — Fri, 18 Jul 2008 14:22:34 +0000

Nice Blog!