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Hypotheses | |
Amyloid-beta and tau protein | |
In Alzheimer's disease, changes in tau protein lead to the disintegration of microtubules in brain cells. | |
The tau hypothesis proposes that tau protein abnormalities initiate the disease cascade.[46] In this model, hyperphosphorylated tau begins to pair with other threads of tau as paired helical filaments. Eventually, they form neurofibrillary tangles inside nerve cell bodies.[65] When this occurs, the microtubules disintegrate, destroying the structure of the cell's cytoskeleton which collapses the neuron's transport system.[66] | |
A number of studies connect the misfolded amyloid beta and tau proteins associated with the pathology of Alzheimer's disease, as bringing about oxidative stress that leads to chronic inflammation.[67] Sustained inflammation (neuroinflammation) is also a feature of other neurodegenerative diseases including Parkinson's disease, and ALS.[68] Spirochete infections have also been linked to dementia.[9] DNA damages accumulate in AD brains; reactive oxygen species may be the major source of this DNA damage.[69] |