The pathophysiology of Alzheimer's disease (AD) is thought to involve the accumulation and deposition of amyloid β (Aβ) peptide in the form of plaques. It is well known that decreased cerebrospinal fluid (CSF) Aβ42 concentrations occur early in AD. Besides this, τ protein becomes hyperphosphorylated (P-τ), getting unstable and unable to bind the microtubules and finally disintegrating into neurofibrillary tangles. The neuropathological process leads to a characteristic pattern of brain damage starting in the medial temporal lobe (MTL) that can be viewed and measured with structural MRI. To read the full article, log in using your NHS OpenAthens details.