Showing posts with label amyloid plaques. Show all posts
Showing posts with label amyloid plaques. Show all posts

Tuesday, 20 August 2013

Now this could be a bit of a breakthrough

The latest Alzheimer Research Newsletter:
http://www.alzforum.org/
contains a fascinating account of research which has found that some people who appear to have Alzheimer's symptoms do not have the biomarkers indicating the presence of amyloid deposits (plaques) which most people with these symptoms do have.

Regular readers of this blog will know that there seems to be a growing scepticism amongst researchers about the almost universally promoted view that the build up of these plaques in the brain constitutes 'the cause' of the disease.

There is also recently reported research which suggests that some of those with the symptoms but not the plaques tend to have a type of dementia that progresses significantly more slowly than the AD which people with symptoms and plaques have.

The question arises: do these groups of people even have the same disease?

As usual, the reports on this site are quite technical.  If anyone can explain these finding more clearly. they are more than welcome to comment.

I have posted prviously about the nuns study
http://adventureswithdementia.blogspot.co.uk/2012/10/possibly-most-exciting-research-into.html

The research discusssed above might begin to explain why some nuns whose brains post-mortem showed no sign of deposits had all the symptoms of AD.  I still await with interest any explanation as to why some nuns had significant deposits but were not, whilst alive, dementia sufferers.

Thursday, 28 February 2013

Looks like a great resource for HSV1 and Alzheimer's

I recently came across this:

http://www.alzforum.org/res/for/journal/detail.asp?liveID=188

It interests me greatly and not just because there is a lot of detail (I've barely scratched the surface) about the link between herpes simplex and Alzheimer's (a link that was first looked at in the 1970's).  I'm also intrigued that what is clearly a reputable Alzheimer's Research site is taking the growing body of research in this area seriously.

I simply cannot understand why the comparable bodies in the UK are neglecting this research.  I think it's scandalous.

Thursday, 29 November 2012

The 'cause' of Alzheimer's is questioned again

I've lost count of the number of times I've read apparently authoritative statements asserting that Alzheimer's disease is caused by the accumulation of amyloid plaques.  This has sometimes been questioned by those who feel that 'tangles' of stuff called 'tau' are a more important cause.  It has also been suggested that the plaques may be the body's attempt to fight the disease.

I've just come across some research that further undermines the conventional view.  Here's the abstract (summary):

According to the “amyloid hypothesis of Alzheimer’s disease,” β-amyloid is the primary driving force in Alzheimer’s disease pathogenesis. Despite the development of many transgenic mouse lines developing abundant β-amyloid-containing plaques in the brain, the actual link between amyloid plaques and neuron loss has not been clearly established, as reports on neuron loss in these models have remained controversial. We investigated transgenic mice expressing human mutant amyloid precursor protein APP751 (KM670/671NL and V717I) and human mutant presenilin-1 (PS-1 M146L). Stereologic and image analyses: revealed substantial age-related neuron loss in the hippocampal pyramidal cell layer of APP/PS-1 double-transgenic mice. The loss of neurons was observed at sites of Aβ aggregation and surrounding astrocytes but, most importantly, was also clearly observed in areas of the parenchyma distant from plaques. These findings point to the potential involvement of more than one mechanism in hippocampal neuron loss in this APP/PS-1 double-transgenic mouse model of Alzheimer’s disease.
(Hippocampal Neuron Loss Exceeds Amyloid Plaque Load in a Transgenic Mouse Model of Alzheimer’s Disease  -  The American Journal of Pathology)

Interestingly this dates from 2004 so perhaps others have pursued it further.  If not, one wonders why not.