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Neuron degeneration, or neurodegeneration, is the progressive loss of structure or function of neurons, which may ultimately lead to neuronal cell death. This biological process is the fundamental pathological feature of numerous neurological disorders, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS) [8, 11]. The process involves a complex cascade of molecular events such as protein misfolding and aggregation, mitochondrial dysfunction, oxidative stress, and chronic neuroinflammation [15, 20]. While 'neuron degeneration' itself is a broad pathological outcome rather than a discrete molecular target like a receptor or enzyme, specific proteins within these pathways serve as viable therapeutic targets. For instance, SARM1 (Sterile alpha and TIR motif-containing protein 1) has been identified as a key molecular executioner of axonal degeneration and is an emerging target for drug development [1, 3]. Current clinical interventions aim to mitigate this process through neuroprotective mechanisms, such as NMDA receptor antagonism, or by using antibodies designed to clear toxic protein aggregates [9, 10]. Monitoring the progression of neuron degeneration is increasingly performed using biomarkers like neurofilament light chain (NfL), which is released into biofluids upon axonal damage [18].
Drugs targeting neurodegenerative processes act through various mechanisms, including NMDA receptor antagonism to prevent excitotoxicity, inhibition of glutamate release, free radical scavenging to reduce oxidative stress, and monoclonal antibody-mediated clearance of protein aggregates like amyloid-beta.
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