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 language | English (US) |
|---|---|
| Pages (from-to) | 140-148 |
| Number of pages | 9 |
| Journal | Journal of Neurochemistry |
| Volume | 120 |
| Issue number | SUPPL. 1 |
| DOIs | |
| State | Published - Jan 2012 |
Keywords
- NMDA receptors
- amyloid β
- glycogen synthase kinase-3
- long-term potentiation
- mammalian target of rapamycin
- reactive oxygen species
ASJC Scopus subject areas
- Biochemistry
- Cellular and Molecular Neuroscience