title: [Significance of intracellular A beta in Alzheimer's disease].
abstract: It is now widely accepted that beta-amyloid has a central role in the pathogenesis of Alzheimer's disease (AD). It is mainly composed of aggregated A beta protein and is deposited in senile plaques and cerebral blood vessels. However, it is not uncommon to see autopsies that reveal significant deposits of beta-amyloid in the brain without manifesting dementia. In fact, several neuropathological studies showed no correlation between beta-amyloid burden and the severity of dementia or loss of synapses. Thus it is questioned whether extracellularly deposited beta-amyloid is directly linked to the Alzheimer pathomechanism. Here I show evidence to support the significance of intraneuronally deposited A beta x-42 by analyzing presenilin 1 transgenic mice and AD patients.
authors.affiliation: National Institute for Longevity Sciences, 36-3, Gengo, Morioka, Obu, 474-8522 Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Tabira
mesh_terms: D000544:Alzheimer Disease / Q000209:etiology* / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000818:Animals; D017209:Apoptosis; D001921:Brain / Q000378:metabolism; D006801:Humans; D008565:Membrane Proteins / Q000235:genetics; D051379:Mice; D008822:Mice, Transgenic; D009474:Neurons / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism*; D058225:Plaque, Amyloid / Q000378:metabolism; D053764:Presenilin-1
chemical_list: D016229:Amyloid beta-Peptides; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D010446:Peptide Fragments; D053764:Presenilin-1; C092862:amyloid beta-protein (10-43)