The<unk>  (AD), also known as the<unk>  hypothesis or the amyloid beta<unk><unk>  hypothesis, is a more recent variant of the amyloid hypothesis of AD, which identifies amyloid beta (Aβ) as the underlying cause of neurotoxicity seen in AD. While the traditional formulation of the amyloid hypothesis pinpoints insoluble, fibrillar aggregates of Aβ as the basis of disruption of calcium<unk>  homeostasis and subsequent apoptosis in AD, the<unk><unk>  hypothesis in 1993 introduced the possibility of an<unk><unk> -forming oligomer of soluble, non-fibrillar Aβ as the cytotoxic species allowing unregulated calcium influx into neurons in AD. The<unk><unk>  hypothesis is broadly supported as an explanation for the calcium<unk>  influx that disrupts calcium<unk>  homeostasis and induces apoptosis in neurons. Because the extracellular deposition of Aβ fibrils in senile plaques is not sufficient to predict risk or onset of AD, and clinical trials of drugs that target the Aβ fibrillization process have largely failed, the<unk><unk>  hypothesis provides novel molecular targets for continued development of AD therapies and for better understanding of the mechanism underlying onset and progression of AD.
Ion channel hypothesis of Alzheimer's disease
Variably protease-sensitive prionopathy
Psychological therapies for dementia
Limbic-predominant age-related TDP-43 encephalopathy
Biochemistry of Alzheimer's disease
Glutamate hypothesis of schizophrenia
Synucleinopathy
Frontotemporal dementia and parkinsonism linked to chromosome 17