Molecular Neurodegeneration Pathways: Amyloid, Tau & Protein Misfolding
Understanding the molecular mechanisms underlying protein misfolding and aggregation is central to advancing therapies for major neurodegenerative disorders. Research on amyloid-beta, tau, alpha-synuclein and TDP-43 has revealed intricate pathways that trigger synaptic loss, metabolic dysfunction, oxidative stress and neuronal death. Structural biology, cryo-EM and proteomics have deepened insights into how toxic oligomers form and propagate across neural networks. Therapeutic strategies now focus on halting misfolding, blocking seeding, enhancing proteostasis and promoting clearance through autophagy and immunotherapy. Anti-amyloid and anti-tau agents, molecular chaperones, gene-silencing technologies and small-molecule stabilizers are under active development. Early detection through molecular biomarkers, including CSF profiles and PET ligands, is enabling more targeted clinical trials. These advances collectively deepen understanding of neurodegenerative cascades and guide the creation of more effective disease-modifying treatments.
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