| First Author | Findley CA | Year | 2019 |
| Journal | ASN Neuro | Volume | 11 |
| Pages | 1759091419855541 | PubMed ID | 31213067 |
| Mgi Jnum | J:277676 | Mgi Id | MGI:6330996 |
| Doi | 10.1177/1759091419855541 | Citation | Findley CA, et al. (2019) Amyloid Beta-Related Alterations to Glutamate Signaling Dynamics During Alzheimer's Disease Progression. ASN Neuro 11:1759091419855541 |
| abstractText | 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 (Ab), rather than insoluble plaques, may instigate synaptic failure. Soluble Ab accumulation results in depression of long-term potentiation leading to cognitive deficits commonly characterized in AD. The mechanisms through which Ab 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 Ab-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. |
