Journal
ASN NEURO
Volume 11, Issue -, Pages -Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1759091419855541
Keywords
alpha 7 nicotinic acetylcholine receptors (alpha 7nAChRs); amyloid oligomers; synaptic dysfunction; excitotoxicity; mild cognitive impairment; N-methyl-D-aspartic acid (NMDA)
Categories
Funding
- National Institute on Aging of the National Institutes of Health [R01AG057767, R01AG061937]
- Illinois Department of Public Health [63282003D, 83282002F]
- Center for Alzheimer's Disease and Related Disorders at Southern Illinois University School of Medicine
- Kenneth Stark Endowment
- American Diabetes Association [1-19-IBS-126]
- Fraternal Order of Eagles
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Alzheimer's disease (AD) ranks sixth on the Centers for Disease Control and Prevention Top 10 Leading Causes of Death list for 2016, and the Alzheimer's Association attributes 60% to 80% of dementia cases as AD related. AD pathology hallmarks include accumulation of senile plaques and neurofibrillary tangles; however, evidence supports that soluble amyloid beta (A beta), rather than insoluble plaques, may instigate synaptic failure. Soluble A beta accumulation results in depression of long-term potentiation leading to cognitive deficits commonly characterized in AD. The mechanisms through which A beta incites cognitive decline have been extensively explored, with a growing body of evidence pointing to modulation of the glutamatergic system. The period of glutamatergic hypoactivation observed alongside long-term potentiation depression and cognitive deficits in later disease stages may be the consequence of a preceding period of increased glutamatergic activity. This review will explore the A beta-related changes to the tripartite glutamate synapse resulting in altered cell signaling throughout disease progression, ultimately culminating in oxidative stress, synaptic dysfunction, and neuronal loss.
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