  I present a theory of Alzheimer's Disease (AD) that explains its symptoms,
pathology, and risk factors. To do this, I introduce a new theory of brain
plasticity that elucidates the physiological roles of AD-related agents. New
events generate synaptic and branching candidates competing for long-term
enhancement. Competition resolution crucially depends on the formation of
membrane lipid rafts, which requires astrocyte-produced cholesterol. Sporadic
AD is caused by impaired formation of plasma membrane lipid rafts, which
prevents the conversion of short- to long-term memory, and yields excessive tau
phosphorylation, intracellular cholesterol accumulation, synaptic dysfunction,
and neurodegeneration. Amyloid beta (Abeta) production is promoted by
cholesterol during the switch to competition resolution, and cholesterol
accumulation stimulates chronic Abeta production, secretion, and aggregation.
The theory addresses all of the major established facts known about the
disease, and is supported by strong evidence.
