Mechanistic review uncovers a protective immunological role for amyloid-β against metals and infections, suggesting late-onset Alzheimer's disease stems from cumulative exposures.
Key Points
To evaluate the hypothesis that amyloid-β functions primarily as a protective immunological and chemical agent rather than an intrinsically neurotoxic driver in Alzheimer's disease.
Synthesized multidisciplinary evidence across biochemistry, coordination chemistry, and immunology.
Evaluated mechanistic relationships between amyloid-β aggregation, transition metal ion binding, and infectious pathogen exposure.
Posits that amyloid-β serves an innate physiological role to sequester toxic metal ions and neutralize infectious pathogens.
Proposes that late-onset Alzheimer's disease results from chronic chemical and biological exposures overwhelming these protective mechanisms rather than amyloid-β toxicity alone.