Divergent Cognitive Status with the Same Braak Stage of Neurofibrillary Pathology: Does the Pattern of Amyloid-β Deposits Make the Difference?

Article type: Short Communication

Authors: Maderna, Emanuela^a | Cattaneo, Cristina^b | Cacciatore, Francesca^a | Catania, Marcella^a | Di Fede, Giuseppe^a | Tagliavini, Fabrizio^a | Giaccone, Giorgio^{a; *}

Affiliations: [a] Fondazione IRCCS Istituto Neurologico Carlo Besta, Milano, Italy | [b] Sezione di Medicina Legale, Dipartimento di Scienze Biomediche per la Salute, University of Milano, Milano, Italy

Correspondence: [*] Correspondence to: Giorgio Giaccone, MD, Fondazione IRCCS Istituto Neurologico Carlo Besta, Milano, via Celoria 11 – 20133 Milano, Italy. Tel.: +39 02 2394 2260; Fax: +39 02 7063 8217; E-mail: giaccone@istituto-besta.it.

Abstract: 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.

Keywords: Alzheimer's disease, amyloid-β, dispersion index, immunohistochemistry, neurofibrillary pathology

DOI: 10.3233/JAD-140540

Journal: Journal of Alzheimer's Disease, vol. 43, no. 2, pp. 375-379, 2015