Regional Overlap of Pathologies in Lewy Body Disorders

Lewy body disorders (LBD) are common neurodegenerative diseases characterized by the presence of aggregated proportional to-synuclein in Lewy bodies and Lewy neurites in the central and peripheral nervous systems. The brains of patients with LBD often display other comor-bid pathologies, i. e. insol...

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Detalles Bibliográficos
Autores: Colom-Cadena, M, Grau-Rivera, O, Planellas, L, Cerquera, C, Morenas, E, Helgueta, S, Munoz, L, Kulisevsky, J, Marti, MJ, Tolosa, E, Clarimon, J, Lleo, A, Gelpi, E
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:España
Institución:Institut d’Investigació Biomèdica Sant Pau (IIB Sant Pau)
Repositorio:r-IIB SANT PAU. Repositorio Institucional de Producción Científica del Instituto de Investigación Biomédica Sant Pau
OAI Identifier:oai:iibsantpau.fundanetsuite.com:p6597
Acceso en línea:https://iibsantpau.fundanetsuite.com/Publicaciones/ProdCientif/PublicacionFrw.aspx?id=6597
Access Level:acceso abierto
Palabra clave:proportional to-Synuclein
beta-Amyloid
Copathology
Dementia with Lewy bodies
Parkinson disease
Parkinson disease dementia
Tau
Descripción
Sumario:Lewy body disorders (LBD) are common neurodegenerative diseases characterized by the presence of aggregated proportional to-synuclein in Lewy bodies and Lewy neurites in the central and peripheral nervous systems. The brains of patients with LBD often display other comor-bid pathologies, i. e. insoluble tau, beta-amyloid aggregates, TAR DNA-binding protein 43 (TDP-43) deposits, and argyrophilic grain disease (AGD). The incidence and physiological relevance of these concurrent pathological findings remain controversial. We per-formed a semiquantitative detailed mapping of proportional to-synuclein, tau, beta-amyloid (A beta), TDP-43, and AGD pathologies in 17 areas in 63 LBD cases (44 with Parkinson disease [PD], 28 with dementia, and 19 with dementia with Lewy bodies). APOE and MAPT genetic variants were also investigated. A majority of LBD cases had 2 or 3 concomitant findings, particularly Alzheimer disease-related pathology. Pathological stages of tau, beta-amyloid and proportional to-synuclein pathologies were increased in cases with dementia. A beta score was the best correlate of the time to dementia in PD. In addition, beta-amyloid deposition correlated with beta-synuclein load in all groups. MAPT H1 haplotype did not influence any assessed pathology in PD. These results highlight the common concurrence of pathologies in patients with LBD that may have an impact on the clinical expression of the diseases.