Mechanisms of glutamate metabolic function and dysfunction in vascular dementia

Abstract

As the global population ages, research on the pathogenesis and treatment options for older patients with dementia has become increasingly important. Vascular dementia (VaD), the second most frequent type of dementia, is characterized by vascular impairment caused by inadequate blood supply to the brain. VaD is a complex neurological disorder involving multiple cells and signaling pathways, and its prevention and treatment pose clinical challenges with significant behavioral implications. Glutamate, the most abundant amino acid in the brain, plays a critical role as an excitatory neurotransmitter, impacting cognitive function, learning, and memory. Abnormal glutamate metabolism has been closely linked to dementia, and reduced blood flow to the brain can lead to excessive glutamate accumulation, resulting in neuronal death. This article highlights the connection between VaD and glutamate metabolism, aiming to identify better methods for preventing and treating VaD via regulating glutamate metabolism.