Controversy - The Cause of
Alzheimer's
By Michael Mullan
Controversy - The Cause of Alzheimer's
By Dr. Michael Mullan
A recent paper by a huge international collaborative group of...
The new gene findings also point to a process called
endocytosis which is the internalization of the cell membrane
typical...
Scientists argue that if a gene such as APOE which has such a
large influence on the population's risk for Alzheimer's has...
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Controversy - The Cause of Alzheimer's / By Michael Mullan

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A recent paper by a huge international collaborative group of researchers has re-fired the controversy over what really causes Alzheimer's disease. An article written by Dr. Michael Mullan, an Alzheimer's researcher.
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Controversy - The Cause of Alzheimer's / By Michael Mullan

  1. 1. Controversy - The Cause of Alzheimer's By Michael Mullan
  2. 2. Controversy - The Cause of Alzheimer's By Dr. Michael Mullan A recent paper by a huge international collaborative group of researchers has re-fired the controversy over what really causes Alzheimer's disease. For many years, researchers have argued that the amyloid protein is the central cause of the disease. However, in commenting on the recent finding, Professor Julie Williams said, "There is something in the immune response which is causing Alzheimer's disease…." according to a BBC report. Dr. Williams' use of the term "causing" is strong language and contrasts sharply with the beliefs of other scientists who promote the "amyloid cascade theory." According to that theory, amyloid is the cause of Alzheimer's disease and brings about the demise of neurons by toxic and inflammatory processes as it accumulates in the brain. In the new findings of 11 more genes associated with Alzheimer's disease (bringing the total to 21), the immune system seems to be implicated. Several other studies have previously implicated the immune system. For instance, a 1999 paper from our own group, published in Science, implicated the molecule CD40 which plays a central role in the immune system. Knocking out CD40 dramatically reduced the amount of amyloid accumulation in transgenic mouse models of Alzheimer's expressing human mutations which trigger early onset disease.
  3. 3. The new gene findings also point to a process called endocytosis which is the internalization of the cell membrane typically after a receptor has been triggered. Interestingly, we have also shown that CD40 triggers endocytosis and, in so doing, it increases the amount of amyloid produced by brain cells. Although the new genetic findings do not give any clear indication of why the immune system may be important, the implication of immune proteins will generate many new theories. Previously, many researchers have noted the role of inflammation and innate immunity in Alzheimer's disease and it may be that these new genetic findings will assist in our understanding of the role of the immune system. However, the sheer size of the study, which according to the BBC website required over 17,000 patients and 37,000 healthy controls, suggests that the effect of some of these genes may be very small. This then naturally gives rise to the question of whether the findings are generalizable to all Alzheimer patients. In addition, the key question of whether any treatments will emerge from these genetic findings is another area hotly debated. Although the genetic role of genes like APP has been known for over 20 years, no therapies have yet been approved which are directed towards the amyloid protein. Similarly, although the APOE gene was implicated in Alzheimer's disease 20 years ago, no treatments have emerged as a consequence.
  4. 4. Scientists argue that if a gene such as APOE which has such a large influence on the population's risk for Alzheimer's has not resulted in a new treatment, why would the discovery of genes of much smaller effect be likely to result in new treatments? However, Professor Williams' comment may suggest that one of the values of such studies is to move the field away from focusing so intently on amyloid towards other potential therapeutic targets. Although the hunt for amyloid therapies has been incessant over the last 20 years, major vaccine studies have failed or shown minimal effect and consequently, researchers are trying to advance anti-amyloid treatments at an early age. Others vehemently oppose this approach, suggesting that amyloid is just the wrong target and that other molecular targets should be sought. Perhaps this new study will switch the focus away from amyloid to the immune and other systems? The origins of Alzheimer's disease have always been hotly debated with researchers taking very strong opinions on the cause of the disease. This intellectual battle seems set to continue with new findings such as those revealed by the present study.

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