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

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

Weiming XiaCenter for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USAAbstract: The development of amyloid-containing neuritic plaques is an invariable characteristic of Alzheimer’s diseases (AD). The c...

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Autor principal: Weiming Xia
Formato: article
Lenguaje:EN
Publicado: Dove Medical Press 2010
Materias:
Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Neurology. Diseases of the nervous system
RC346-429
Acceso en línea:https://doaj.org/article/319cf29a66cc4c8fb0a26688ef7a724f
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spelling oai:doaj.org-article:319cf29a66cc4c8fb0a26688ef7a724f2021-12-02T03:13:09ZBrain amyloid β protein and memory disruption in Alzheimer’s disease1176-63281178-2021https://doaj.org/article/319cf29a66cc4c8fb0a26688ef7a724f2010-09-01T00:00:00Zhttp://www.dovepress.com/brain-amyloid-szlig-protein-and-memory-disruption-in-alzheimerrsquos-d-a5236https://doaj.org/toc/1176-6328https://doaj.org/toc/1178-2021Weiming XiaCenter for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USAAbstract: 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 Aß 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.Keywords: Alzheimer, amyloid, oligomer, long-term potentiation, NMDA Weiming XiaDove Medical PressarticleNeurosciences. Biological psychiatry. NeuropsychiatryRC321-571Neurology. Diseases of the nervous systemRC346-429ENNeuropsychiatric Disease and Treatment, Vol 2010, Iss Issue 1, Pp 605-612 (2010)
institution DOAJ
collection DOAJ
language EN
topic Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Neurology. Diseases of the nervous system
RC346-429
spellingShingle Neurosciences. Biological psychiatry. Neuropsychiatry
RC321-571
Neurology. Diseases of the nervous system
RC346-429
Weiming Xia
Brain amyloid β protein and memory disruption in Alzheimer’s disease
description Weiming XiaCenter for Neurologic Diseases, Department of Neurology, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USAAbstract: 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 Aß 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.Keywords: Alzheimer, amyloid, oligomer, long-term potentiation, NMDA
format article
author Weiming Xia
author_facet Weiming Xia
author_sort Weiming Xia
title Brain amyloid β protein and memory disruption in Alzheimer’s disease
title_short Brain amyloid β protein and memory disruption in Alzheimer’s disease
title_full Brain amyloid β protein and memory disruption in Alzheimer’s disease
title_fullStr Brain amyloid β protein and memory disruption in Alzheimer’s disease
title_full_unstemmed Brain amyloid β protein and memory disruption in Alzheimer’s disease
title_sort brain amyloid β protein and memory disruption in alzheimer’s disease
publisher Dove Medical Press
publishDate 2010
url https://doaj.org/article/319cf29a66cc4c8fb0a26688ef7a724f
work_keys_str_mv AT weimingxia brainamyloidampbetaproteinandmemorydisruptioninalzheimeramprsquosdisease
_version_ 1718401844585168896

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