No wonder people are confused

I'm sceptical about this article and not just because it's in the Daily Mail:

http://www.dailymail.co.uk/news/article-3413873/Alzheimer-s-cause-discovered-Poisonous-algae-freshwater-lakes-reservoirs-UK-fuelling-dementia-epidemic-afflicting-1m-people.html#ixzz3y9MDkzK4

I also read in latest issue of 'The Week' an article which quotes Professor John Hardy telling the Royal Society about 'drugs to halt AD within a decade'. The Week article and also contains this 'fact' (though it's not clear where it comes from):

Since 1980, there has been a 20% drop in dementia incidence (in Britain), possibly as a result of people taking actions to reduce their cholesterol levels.

I've never seen this before and most statistics suggest a growing problem. The Mail article talks of 'increasing rates of Alzheimer's'.

And even if it is true I think his possible reason is pretty implausible.

So much of the stuff you read about AD, even when you discount the massive amount of obvious twaddle, contradicts other stuff. And the media never delve into these matters in any detail at all but just wait for the next press release to come along.

Finally, so many of the articles and news items talk about dementia and Alzheimer's as if they are one condition with one cause (whatever that happens to be this week).

Pure ignorance across the board.

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.

Possibly the most exciting research into dementia so far

It's not new. I've posted previously about the nuns' study:
http://adventureswithdementia.blogspot.co.uk/2012/05/nuns-study.html

I have found an article that explains, more clearly than ever, why this research should receive so much more attention:

Perhaps the single most important conclusion from the study is that Alzheimer disease is not straight forward. In several cases, pathology studies of brain tissue from the deceased nuns did not correlate with their performance on cognitive function tests. Sometimes the pathologist would score a brain as having signs of extremely advanced AD, only to learn later that the nun herself scored extremely well on all cognitive tests. Other times a brain would show only slight damage associated with AD, and the nun was characterized as exhibiting the signs of advanced cognitive decline and dementia.

I often wonder whether there is anything new from this study. Apparently the original researcher has retired but the University of Minnesota is hoping to continue the work:

Additionally, the University of Minnesota has announced that it will begin a second study, with a new group of volunteer nuns, to delve further into the mysteries of Alzheimer disease: Why do some people develop symptoms and not others? Why do some people with advanced brain damage: plaques, tangles and tissue loss, not show any symptoms, while others with minimal brain damage show symptoms of advanced AD?

How odd that these questions are so rarely referred to in discussions of the disease!

Here's a link to the article:
http://promega.wordpress.com/2009/05/04/alzheimer-disease-and-the-nun-study/

Could this be the answer?

This suggestion may help some people. In the long run. Unfortunately, George Monbiot who wrote the article says he has had the greatest difficulty understanding some of the research so I reckon most of us will have to take it on trust for the time being.

http://www.guardian.co.uk/commentisfree/2012/sep/10/alzheimers-junk-food-catastrophic-effect

My worry would be that, whilst the suggested cause could well be applicable in some cases, or at least be a contributory factor, one can see how all people with dementia might be branded as consumers of junk food. Blaming the victim is all too common in matters of health, particularly where the media are concerned.