On of those more complex posts. I'm afraid.....

....but give it a go.  I'm not for one moment claiming to understand it properly, but I am excited by what it appears to suggest.  The researchers believe that they have found why some people with significant plaques and tangles in their brains do not develop dementia (see nuns study).

Note also the first comment at the end of the main article where the writer states as if it is well known that:  'A sizable proportion of elderly individuals with substantial AD pathology does not appear to progress to dementia...'  You would not think it was well-known judging by the number of times 'the causes of dementia' are discussed without this key fact being mentioned.

Perhaps there is some research hidden away somewhere that explains why some people who have few or no plaques and tangles do develop dementia (i.e. the other side of the nuns study coin)?

Here is the link:
http://www.alzforum.org/news/research-news/no-rest-weary-neurons-protective-factor-stems-cognitive-decline?utm_source=Alzforum+Newsletter+03%2F24%2F2014&utm_campaign=Alzforum+Newsletter+3%2F24%2F14&utm_medium=email

I would welcome comments, particularly from any researchers.

What's in a name?

The Alzheimer's Society seems to be renaming itself 'Alzheimer's Society' (i.e. dropping the definite article). Of course they may do what they like with their own name but it may not catch on.

An employee of AS was recently interviewed on the BBC and was introduced using the new name.  He then used the new name, but it's obviously unnatural, even to an employee, and later he used the old name.  When the interview finished, the presenter who'd introduced him reverted to the old name herself.

In any case, I am puzzled as to why Alois Alzheimer's name is still attached to the disease.  He was the first person to diagnose a case of what we would now call early/young onset Alzheimer's Disase.  Interestingly, he distinguished the disease from 'pre-senile dementia', indicating that dementia was recognised as a common problem as people got older but previously not recognised properly in younger people.

Alzheimer examined the brain of his patient post-mortem and sketched pictures of the plaques and tangles.  Decades later these were recognised as more or less identical to the plaques and tangles seen when the brains of elderly senile patients were examined.  It was decided they had the same disease.

Yet as time has passed it's become clearer that there are many, many, diseases that cause dementia.  Some of them are similar to each other and some of them are not. In general public discussion 'dementia' and 'Alzheimer's disease' are used interchangeably which is not helpful.

Equally, it is assumed that the plaques and tangles are always a marker of the disease and a great deal of research has been devoted to trying to remove the plaques and tangles.

Yet as the not-famous-enough nuns study shows some people have the plaques and tangles but don't have dementia and some people have dementia but do not have significant plaques and tangles.

It's possible that the emphasis of much research has been misplaced and that other possible research areas are being overlooked.

So how helpful is it that Alzheimer's name is still so well-known?

And to end where we began, it's probably time for the Alzheimer's Society to adopt a more sensible name.  Or, better still, lead a move towards the amalgamation of the various dementia charities.  One national dementia charity could become very influential.

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.