NDLI: Brain amyloid β protein and memory disruption in Alzheimer’s disease

Content Provider	PubMed Central
Author	Xia, Weiming
Abstract	The development of amyloid-containing neuritic plaques is an invariable characteristic of Alzheimer’s diseases (AD). The conversion from monomeric amyloid β protein (Aβ) to oligomeric Aβ and finally neuritic plaques is highly dynamic. The specific Aβ species that is correlated with disease severity remains to be discovered. Oligomeric Aβ has been detected in cultured cells, rodent and human brains, as well as human cerebrospinal fluid. Synthetic, cell, and brain derived Aβ oligomers have been found to inhibit hippocampal long-term potentiation (LTP) and this effect can be suppressed by the blockage of Aβ oligomer formation. A large body of evidence suggests that Aβ oligomers inhibit N-methyl-D-aspartate receptor dependent LTP; additional receptors have also been found to elicit downstream pathways upon binding to Aβ oligomers. Amyloid antibodies and small molecular compounds that reduce brain Aβ levels and block Aβ oligomer formation are capable of reversing synaptic dysfunction and these approaches hold a promising therapeutic potential to rescue memory disruption.
Related Links	http://dx.doi.org/10.2147/ndt.s7460
Ending Page	611
Page Count	7
Starting Page	605
File Format	PDF
ISSN	11766328
e-ISSN	11782021
Journal	Neuropsychiatric Disease and Treatment
Volume Number	6
Language	English
Publisher	Dove Medical Press
Publisher Date	2010-09-01
Access Restriction	Open
Rights Holder	Dove Medical Press
Subject Keyword	Biological Psychiatry Psychiatry and Mental health Research in Higher Education
Content Type	Text
Resource Type	Article

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