Abstract |
Alzheimer's disease (AD) is the most common form of dementia, which is characterized by the neuropathological accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles (NFTs). Clinically, patients will endure a gradual erosion of memory and other higher order cognitive functions. Whilst the underlying etiology of the disease remains to be definitively identified, a body of work has developed over the last two decades demonstrating that AD plasma/serum and brain are characterized by a dyshomeostasis in a number of metal ions. Furthermore, these metals (such as zinc, copper and iron) play roles in the regulation of the levels of AD-related proteins, including the amyloid precursor protein (APP) and tau. It is becoming apparent that metals also interact with other proteins, including apolipoprotein E ( ApoE). The Apolipoprotein E gene ( APOE) is critically associated with AD, with APOE4 representing the strongest genetic risk factor for the development of late-onset AD. In this review we will summarize the evidence supporting a role for metals in the function of ApoE and its consequent role in the pathogenesis of AD.
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Authors | He Xu, David I Finkelstein, Paul A Adlard |
Journal | Frontiers in aging neuroscience
(Front Aging Neurosci)
Vol. 6
Pg. 121
( 2014)
ISSN: 1663-4365 [Print] Switzerland |
PMID | 24971061
(Publication Type: Journal Article, Review)
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