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Amyloid deposits are insoluble fibrillar aggregates of misfolded proteins that accumulate in tissues and organs, disrupting normal structure and function. They are characteristic of a group of diseases called amyloidoses, which can be systemic or localized. Each amyloidosis subtype is defined by the precursor protein forming the fibrils: common variants include immunoglobulin light chains (AL amyloidosis), serum amyloid A (AA amyloidosis), transthyretin (ATTR, in familial or senile amyloidosis), and amyloid-beta (Aβ, in Alzheimer's disease). Diagnosis relies on tissue biopsy and specialized staining (Congo red), while therapy aims to reduce precursor protein production and clear deposits. Amyloid accumulation is linked to severe, often multisystem disease, and disease management involves both direct and indirect targeting of underlying protein misfolding and deposition.
Inhibit precursor protein production (e.g., stabilize or silence genes); Facilitate clearance or reduce aggregation of amyloid fibrils; Immunotherapy (experimental: antibodies to remove deposits).
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