Amyloid β

linking synaptic plasticity failure to memory disruption in Alzheimer's disease

Tao Ma, Eric Klann

Research output: Contribution to journalArticle

Abstract

Mounting evidence suggests that amyloid beta-induced impairments in synaptic plasticity that is accompanied by cognitive decline and dementia represent key pathogenic steps of Alzheimer's disease. In this study, we review recent advances in the study of the molecular and cellular mechanisms underlying Alzheimer's disease-associated synaptic dysfunction and memory deficits, and how these mechanisms could provide novel avenues for therapeutic intervention to treat this devastating neurodegenerative disease.

Original languageEnglish (US)
Pages (from-to)140-148
Number of pages9
JournalJournal of Neurochemistry
Volume120
Issue numberSUPPL. 1
DOIs
StatePublished - Jan 2012

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Neuronal Plasticity
Amyloid
Plasticity
Alzheimer Disease
Neurodegenerative diseases
Data storage equipment
Memory Disorders
Mountings
Neurodegenerative Diseases
Dementia
Therapeutics
Cognitive Dysfunction

Keywords

  • amyloid β
  • glycogen synthase kinase-3
  • long-term potentiation
  • mammalian target of rapamycin
  • NMDA receptors
  • reactive oxygen species

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Cite this

Amyloid β : linking synaptic plasticity failure to memory disruption in Alzheimer's disease. / Ma, Tao; Klann, Eric.

In: Journal of Neurochemistry, Vol. 120, No. SUPPL. 1, 01.2012, p. 140-148.

Research output: Contribution to journalArticle

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