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Association between naturally occurring antiamyloid β autoantibodies and medial temporal lobe atrophy in Alzheimer's disease
  1. Manuel Menendez-Gonzalez1,2
  1. 1Department of Neurology, Hospital Universitario Central de Asturias, Oviedo, Asturias, Spain
  2. 2Department of Morphology and Cellular Biology, Universidad de Oviedo, Oviedo, Asturias, Spain
  1. Correspondence to Dr Manuel, Menendez-Gonzalez, Department of Neurology, Hospital Universitario Central de Asturias, Oviedo 33011, Spain; manuelmenendez{at}gmail.com

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Editorial commentary

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 …

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