Literature: A-K ; L-Z ; subject area
Compiled by: Julian Thorpe
Causes
|
Please Note: Due to time constraints, the text part of this page has not been updated for some time. However, references are added reasonably frequently. |
AD is initiated by factors that may be genetic or environmental
in nature.
 | The former include mutations in the amyloid protein precursor (APP) gene on chromosome 21 and in the two presenilin genes on chromosomes 14 (presenilin-1) and 1 (presenilin-2) which give rise to the familial early-onset forms of the disease (e.g. see Chapman et al., 2001). |
| In the vast majority of cases, however, AD is of the sporadic, late-onset form brought about by the so-called ‘susceptibility’ apolipoprotein E gene (allelic variant 4 on chromosome 19; Mahley and Rall, 2000 ) or by mitochondrial mutations and polymorphisms ( Orth and Schapira, 2001). |
| Pin1 protein: polymorphisms in the Pin1 promoter have recently been identified which result in decreased protein expression and correlate with AD (Segat et al., In Press). |
| Environmental risk factors are generally considered to be more
contentious , but may include head trauma (Plassman et al., 2000
) and heavy metals such as aluminium (Campbell et al., 2001
, Civita et al., 2002, Flaten, 2001, Jones et al., 1998
), iron (Pinero and Connor, 2000 ) and zinc ( Park et al.,
2001 ). |
Please go to David Small's
Alzheimer Web Page
for excellent further background on this aspect.
And have a look at: the
genetic aspects
of AD (courtesy of the
Alzheimer Research Forum
) or Genes and Alzheimer's Disease
(a review by Benjamin Wolozin
, Loyola University, Chicago) or the
NCBI site Genes and Disease (Alzheimer's)
.
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