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 |
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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 journal › Article
}
TY - JOUR
T1 - Amyloid β
T2 - linking synaptic plasticity failure to memory disruption in Alzheimer's disease
AU - Ma, Tao
AU - Klann, Eric
PY - 2012/1
Y1 - 2012/1
N2 - 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.
AB - 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.
KW - amyloid β
KW - glycogen synthase kinase-3
KW - long-term potentiation
KW - mammalian target of rapamycin
KW - NMDA receptors
KW - reactive oxygen species
UR - http://www.scopus.com/inward/record.url?scp=84655160769&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84655160769&partnerID=8YFLogxK
U2 - 10.1111/j.1471-4159.2011.07506.x
DO - 10.1111/j.1471-4159.2011.07506.x
M3 - Article
C2 - 22122128
AN - SCOPUS:84655160769
VL - 120
SP - 140
EP - 148
JO - Journal of Neurochemistry
JF - Journal of Neurochemistry
SN - 0022-3042
IS - SUPPL. 1
ER -