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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. Both CSF biomarkers (Aβ and P-τ) and MTL atrophy have been accepted as biomarkers of AD, supporting the diagnosis of AD even in preclinical stages.1 There is some correlation between MRI findings and CSF biomarkers. On one hand, atrophy of the MTL is a diagnostic marker for AD at the mild cognitive impairment stage, although this is not a such …
Correction Notice This article has been corrected since it published Online First. The title has been corrected.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.
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