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EDITORIAL LZHEIMER DISEASE (AD) IS A NEURODEGEN- onset AD. Discovery of many missense familial AD mu- erative disease characterized by a decline tations in APP and the presenilin 1 and presenilin 2 genes in cognitive function. The two major have further strengthened the support for the role of A pathological features of this disease in- in AD. These familial AD mutations sometimes increase A clude extracellular-amyloid (A) plaques total A levels but more frequently increase the ratio of and intraneural neurofibrillary tangles. These pathologi- A to A , pointing to a critical role of A in AD patho- 42 40 42 cal features seem to appear years before cognitive symp- genesis. In addition, A deposits are more abundant in toms. Several hypotheses relate the pathological deterio- those patients with AD with the heritable ε4 allele of apo- rations in the brain of patients with AD to the mechanisms lipoprotein E than in ε4-negative individuals. of neural degeneration. Among them, the amyloid hy- Deposition of A alone, however, is inadequate to ex- pothesis has emerged as a critical determinant of this pa- plain the disease—there is an inconsistent relationship be- thology. According to this hypothesis, the neural degen- tween the
JAMA Neurology – American Medical Association
Published: Jul 1, 2008
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