Revisiting the role of amyloid-β: A molecular and immunological perspective

Alzheimer's disease (AD) affects about fifty million people worldwide. Its main characteristics are the formation of amyloid deposits and of neurofibrillary tangles, and cognition loss. To date, no clear etiology for this disease has been identified. Metal ions have been shown to accumulate in amyloid deposits. Moreover, multiple infections have been shown to be risk factors for the development of AD and other dementia, with vaccines playing protective roles. I will here elaborate on the likelihood that amyloid-β is not dominantly a toxic molecule, but a protective protein fragment. A combination of chemical and biological exposures, with metals and infections playing key roles, would be essential factors in late-onset cases of AD. A new, translational mechanistic proposal is presented here, combining abundant experimental results and ideas from the fields of biochemistry, coordination chemistry and immunology.