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Int. J. Mol. Sci. 2016, 17(2), 206; doi:10.3390/ijms17020206

Genetic and Transcriptomic Profiles of Inflammation in Neurodegenerative Diseases: Alzheimer, Parkinson, Creutzfeldt-Jakob and Tauopathies

1
Institute of Neuropathology, Bellvitge University Hospital, IDIBELL, Barcelona 08034, Spain
2
CIBERNED (Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas), Institute Carlos III, Madrid 28029, Spain
3
Department of Pathology and Experimental Therapeutics, University of Barcelona, 08907 Hospitalet de Llobregat, Barcelona 08034, Spain
*
Author to whom correspondence should be addressed.
Academic Editor: Xiaofeng Jia
Received: 4 October 2015 / Revised: 21 January 2016 / Accepted: 25 January 2016 / Published: 4 February 2016
(This article belongs to the Special Issue Mechanisms of Neurodegeneration)
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Abstract

Polymorphisms in certain inflammatory-related genes have been identified as putative differential risk factors of neurodegenerative diseases with abnormal protein aggregates, such as sporadic Alzheimer’s disease (AD) and sporadic Parkinson’s disease (sPD). Gene expression studies of cytokines and mediators of the immune response have been made in post-mortem human brain samples in AD, sPD, sporadic Creutzfeldt-Jakob disease (sCJD) subtypes MM1 and VV2, Pick’s disease (PiD), progressive supranuclear palsy (PSP) and frontotemporal lobar degeneration linked to mutation P301L in MAPT Frontotemporal lobar degeneration-tau (FTLD-tau). The studies have disclosed variable gene regulation which is: (1) disease-dependent in the frontal cortex area 8 in AD, sPD, sCJD MM1 and VV2, PiD, PSP and FTLD-tau; (2) region-dependent as seen when comparing the entorhinal cortex, orbitofrontal cortex, and frontal cortex area 8 (FC) in AD; the substantia nigra, putamen, FC, and angular gyrus in PD, as well as the FC and cerebellum in sCJD; (3) genotype-dependent as seen considering sCJD MM1 and VV2; and (4) stage-dependent as seen in AD at different stages of disease progression. These observations show that regulation of inflammation is much more complicated and diverse than currently understood, and that new therapeutic approaches must be designed in order to selectively act on specific targets in particular diseases and at different time points of disease progression. View Full-Text
Keywords: inflammation; microglia; cytokines; complement; toll-like receptors; chemokines; Alzheimer’s disease; Parkinson’s disease; Creutzfeldt-Jakob’s disease; tauopathies inflammation; microglia; cytokines; complement; toll-like receptors; chemokines; Alzheimer’s disease; Parkinson’s disease; Creutzfeldt-Jakob’s disease; tauopathies
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López González, I.; Garcia-Esparcia, P.; Llorens, F.; Ferrer, I. Genetic and Transcriptomic Profiles of Inflammation in Neurodegenerative Diseases: Alzheimer, Parkinson, Creutzfeldt-Jakob and Tauopathies. Int. J. Mol. Sci. 2016, 17, 206.

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