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What causes Alzheimer disease?

By definition, all forms of Alzheimer disease share two features in common, namely the abnormal accumulation of two misfolded proteins: 1) beta-amyloid (a-beta) and 2) phosphorylated tau (p-tau). The accumulation of these proteins may result from either over-production in or decreased clearance from the brain.

A-beta amyloid proteins accumulate at synapses (sites of inter-neuronal communications) to form amyloid plaques. This process jams the communication of information within complex networks of brain cells. Communication normally involves the release of chemical neurotransmitters from the endings of one nerve cells (pre-synaptic terminals), which then dock at receptors of receiving nerve cells (post-synaptic terminals).

P-tau form helical filaments which are known as “neurofibrillary tangles” within the neuron cell body and “neurites” at nerve cell terminals. This causes problems in the vital transportation of molecules within the nerve cell, which takes place through a system of microtubules akin to those that transport water and nutrients to the leaves of plants and trees.

Billions of neurons and trillions of synapses in the human brain are organized in complex networks specialized for sensory perception and movement, as well as memory and intellectual processing (higher cognitive functions). The networks for higher cognitive function suffer the brunt of damage in Alzheimer disease.