Dysregulated Neurotransmission and the Role of Viruses in Alzheimer's Disease

神经递质传递失调及病毒在阿尔茨海默病中的作用

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Abstract

The causes of neurodegeneration remain elusive. There is growing evidence linking viral infection to dysregulated neurotransmission as a causative factor in Alzheimer's disease. Studies suggest that viral infection may result in dysregulated glutamatergic and l-arginine/NO neurotransmission that can initiate neurodegeneration and neuroinflammation within AD. This involves viral infection (HIV-1/HSV-1) altering glutamate biosynthesis and receptor activation resulting in excessive influxes of glutamate and subsequent dysregulation of Ca(2+) influx that all contribute to reduced dendrite growth and tau phosphorylation. For l-arginine/NO neurotransmission, the mechanism derives from the "protective" antiviral mechanisms of NO that correlate with pathologies such as β-amyloid peptide accumulation and functional degeneration of hippocampal neurons, respectively. More research is required to underpin the direct mechanisms that viruses might impact to induce specific pathologies.

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