The neuropathological hallmark of Alzheimer's disease (AD) is the co-occurrence of extracellular amyloid-β (Aβ) deposition and intraneuronal neurofibrillary changes composed of abnormal tau. Over the last decades, the concept emerged that neurofibrillary changes progress in a hierarchical manner from mesial temporal structures through the associative neocortex to primary sensory and motor fields, paralleling cognitive deterioration closer than Aβ. The observation that two patients (one cognitively normal, one with dementia) exhibited neurofibrillary changes closely overlapping as regards their entity and topographic distribution but differed for characteristics of Aβ deposition suggests that the latter may directly contribute in determining cognitive impairment in AD.
|Titolo:||Divergent cognitive status with the same braak stage of neurofibrillary pathology : does the pattern of amyloid-β deposits make the difference?|
CATTANEO, CRISTINA (Secondo)
|Parole Chiave:||Alzheimer's disease; amyloid-β; dispersion index; immunohistochemistry; neurofibrillary pathology; Aged; Aged, 80 and over; Alzheimer Disease; Amyloid beta-Peptides; Autopsy; Cognition Disorders; Disease Progression; Female; Humans; Neurofibrillary Tangles; Psychiatric Status Rating Scales; Psychiatry and Mental Health; Geriatrics and Gerontology; Clinical Psychology; Medicine (all)|
|Settore Scientifico Disciplinare:||Settore MED/43 - Medicina Legale|
|Data di pubblicazione:||2015|
|Digital Object Identifier (DOI):||10.3233/JAD-140540|
|Appare nelle tipologie:||01 - Articolo su periodico|