Why does neuronal damage continue in some neurodegenerative diseases even after the initial triggering event?

💡 Explanation

Misfolded proteins, like amyloid-beta or tau, can aggregate and act as seeds, inducing further misfolding and aggregation of native proteins; this process is known as seeding. Because of this prion-like propagation mechanism, protein aggregation continues, therefore damage persists, rather than halting, even after the initial trigger is removed.

• Why does significant muscle sarcopenia during aging impair glucose tolerance more than simple disuse atrophy?
• Why does cartilage breakdown accelerate in an osteoarthritic knee joint under high compressive loads?
• Why does thyroid hormone (T4) production decrease when iodine intake acutely drops below the minimum required for thyroglobulin iodination?
• Following meniscus removal with knee osteoarthritis, what action accelerates osteophyte formation?
• Why does diabetes insipidus often result in increased serum osmolality and dehydration?
• Why does severe insulin resistance often coincide with elevated triglyceride levels in patients with metabolic syndrome?