Friend or Foe? Defining the Role of Glutamate in Aging and Alzheimer’s Disease

Frontiers in Aging

MaKayla F. Cox¹  Kevin N. Hascup³  Andrzej Bartke³  Erin R. Hascup⁴ 

[1] Dale and Deborah Smith Center for Alzheimer’s Research and Treatment, Department of Neurology, Neurosciences Institute, Southern Illinois University School of Medicine, Springfield, IL, United States;Department of Internal Medicine, Southern Illinois University School of Medicine, Springfield, IL, United States;Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL, United States;Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL, United States;

关键词: excitotoxcity;    neurodegenerative disease;    amyloid—beta;    geroscience;    biomarker;    hippocampus;   

DOI  :  10.3389/fragi.2022.929474

来源: DOAJ

【 摘 要 】

Aging is a naturally occurring decline of physiological processes and biological pathways that affects both the structural and functional integrity of the body and brain. These physiological changes reduce motor skills, executive function, memory recall, and processing speeds. Aging is also a major risk factor for multiple neurodegenerative disorders including Alzheimer’s disease (AD). Identifying a biomarker, or biomarkers, that signals the transition from physiological to pathological aging would aid in earlier therapeutic options or interventional strategies. Considering the importance of glutamate signaling in synaptic plasticity, motor movement, and cognition, this neurotransmitter serves as a juncture between cognitive health and disease. This article discusses glutamatergic signaling during physiological aging and the pathological changes observed in AD patients. Findings from studies in mouse models of successful aging and AD are reviewed and provide a biological context for this transition. Finally, current techniques to monitor brain glutamate are highlighted. These techniques may aid in elucidating time-point specific therapeutic windows to modify disease outcome.

【 授权许可】

Unknown