Abstract
Alzheimer's disease (AD) is a multifactorial entity with a complex pathogeny. Recent findings on this subject are discussed in this article, centering mainly on genetic factors, cerebral ischemia and their association with the most typical histologic lesions in AD. Finally, a hypothetical model is proposed, in which beta-amyloid represents the key element.
MeSH terms
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Alzheimer Disease / etiology*
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Alzheimer Disease / genetics
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Alzheimer Disease / metabolism
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Alzheimer Disease / pathology
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Amyloid beta-Peptides / metabolism
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Amyloid beta-Protein Precursor / genetics
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Amyloid beta-Protein Precursor / metabolism
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Apolipoproteins E / metabolism
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Apoptosis
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Brain Ischemia / complications
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Humans
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Membrane Lipids / metabolism
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Membrane Proteins / genetics
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Membrane Proteins / physiology
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Models, Neurological
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Nerve Tissue Proteins / metabolism
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Neurofibrillary Tangles
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Phosphorylation
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Presenilin-1
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Presenilin-2
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Protein Processing, Post-Translational
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tau Proteins / metabolism
Substances
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Amyloid beta-Peptides
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Amyloid beta-Protein Precursor
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Apolipoproteins E
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Membrane Lipids
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Membrane Proteins
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Nerve Tissue Proteins
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PSEN1 protein, human
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PSEN2 protein, human
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Presenilin-1
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Presenilin-2
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tau Proteins