Comorbidities

• Published in: Handbook of Clinical Neurology Vol. 145; pp. 573 - 577
• Main Authors: Alafuzoff, Irina, Kovacs, Gabor G.
• Format: Book Chapter Journal Article
• Language: English
• Published: Netherlands Elsevier Health Sciences 01.01.2018
• Subjects: alpha-Synuclein - metabolism; altered proteins; Amyloid beta-Peptides - metabolism; Brain - metabolism; Brain - pathology; Brain Diseases - epidemiology; Brain Diseases - metabolism; Brain Diseases - pathology; Comorbidity; DNA-Binding Proteins - metabolism; Humans; hyperphosphorylated τ; Pathology; Patologi; transactive DNA binding protein 43; vascular lesions; α-synuclin; β-amyloid; hyperphosphorylated τ; α-synuclin; altered proteins; vascular lesions; transactive DNA binding protein 43; β-amyloid
• ISBN: 0128023953; 9780128023952
• ISSN: 0072-9752; 2212-4152
• DOI: 10.1016/B978-0-12-802395-2.00036-5

The term comorbidities or mixed pathologies is used when brain tissue, a surgical sample, or postmortem brain displays a mixture of protein alterations or other pathologies. Most of the alterations when seen in sufficient extent are considered causative, are related to a certain clinical phenotype, i.e., when hyperphosphorylated τ (HPτ) is observed in occipital cortex concomitant with β-amyloid (Aβ), the diagnosis is Alzheimer disease (AD). When HPτ is observed in hippocampal structures in a subject with extensive and widespread α-synuclein pathology, a Lewy body disease (LBD), the HPτ pathology is considered as a concomitant alteration. There are numerous reports indicating that when “concomitant” pathologies are seen in a subject with certain neurodegenerative diseases, the clinical phenotype might be altered. In addition there are those cases where many alterations are seen in a sparse extent, but jointly they lead to a clinical syndrome. Thus today it is not sufficient to confirm a certain pathology to be seen, i.e., AD- or LBD-related; in addition the concomitant aging-related alterations have to be looked for.