Mechanisms are the biological processes that explain how stress, injury, or genetic factors turn into cellular dysfunction and disease. A mutation may begin the process, or a stressor like chemotherapy or head trauma may trigger it, but the disease itself unfolds through mechanisms: mitochondria fail to meet energy demands, proteins misfold and aggregate, lysosomes struggle to clear damaged material, immune cells become chronically activated, axons degenerate. These mechanisms bridge the cause and the symptoms a patient eventually experiences.

Several terms appear repeatedly across neurodegeneration. Mitochondrial dysfunction refers to failure of the cell’s energy and metabolic systems. Oxidative stress occurs when reactive molecules damage proteins, lipids, or DNA faster than the cell can repair them. Protein aggregation is when proteins lose their normal shape and clump together, as seen with amyloid, tau, alpha-synuclein, TDP-43, or mutant huntingtin. Autophagy and lysosomal function manage the cell’s recycling and waste-disposal systems. Inflammation refers to immune activation that may begin as protective but become damaging when chronic. These mechanisms often overlap, creating cycles of stress that gradually overwhelm vulnerable neurons and supporting cells (glia).