Journal Article (Review Article)

DZNE-2020-04173

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Neuroinflammation in Alzheimer's disease.

Heneka, M. (First author)DZNE* ; Carson, M. J. ; El Khoury, J. ; Landreth, G. E. ; Brosseron, F.DZNE* ; Feinstein, D. L. ; Jacobs, A. H. ; Wyss-Coray, T. ; Vitorica, J. ; Ransohoff, R. M. ; Herrup, K. ; Frautschy, S. A. ; Finsen, B. ; Brown, G. C. ; Verkhratsky, A. ; Yamanaka, K. ; Koistinaho, J. ; Latz, E.DZNE* ; Halle, A. ; Petzold, G. C.DZNE* ; Town, T. ; Morgan, D. ; Shinohara, M. L. ; Perry, V. H. ; Holmes, C. ; Bazan, N. G. ; Brooks, D. J. ; Hunot, S. ; Joseph, B. ; Deigendesch, N. ; Garaschuk, O. ; Boddeke, E. ; Dinarello, C. A. ; Breitner, J. C. ; Cole, G. M. ; Golenbock, D. T. ; Kummer, M. P.

2015
Lancet Publ. Group London

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Please use a persistent id in citations: doi:10.1016/S1474-4422(15)70016-5

Abstract: Increasing evidence suggests that Alzheimer's disease pathogenesis is not restricted to the neuronal compartment, but includes strong interactions with immunological mechanisms in the brain. Misfolded and aggregated proteins bind to pattern recognition receptors on microglia and astroglia, and trigger an innate immune response characterised by release of inflammatory mediators, which contribute to disease progression and severity. Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction. External factors, including systemic inflammation and obesity, are likely to interfere with immunological processes of the brain and further promote disease progression. Modulation of risk factors and targeting of these immune mechanisms could lead to future therapeutic or preventive strategies for Alzheimer's disease.

Keyword(s): Alzheimer Disease: genetics (MeSH) ; Alzheimer Disease: immunology (MeSH) ; Alzheimer Disease: metabolism (MeSH) ; Alzheimer Disease: pathology (MeSH) ; Alzheimer Disease: prevention & control (MeSH) ; Animals (MeSH) ; Anti-Inflammatory Agents, Non-Steroidal: therapeutic use (MeSH) ; Astrocytes: immunology (MeSH) ; Astrocytes: pathology (MeSH) ; Biomarkers: blood (MeSH) ; Biomarkers: cerebrospinal fluid (MeSH) ; Brain Injuries: complications (MeSH) ; Brain Injuries: metabolism (MeSH) ; Clinical Trials as Topic (MeSH) ; Disease Models, Animal (MeSH) ; Disease Progression (MeSH) ; Humans (MeSH) ; Immunity, Innate (MeSH) ; Immunization (MeSH) ; Inflammation: diagnosis (MeSH) ; Inflammation: immunology (MeSH) ; Inflammation: metabolism (MeSH) ; Inflammation Mediators: immunology (MeSH) ; Inflammation Mediators: metabolism (MeSH) ; Locus Coeruleus: pathology (MeSH) ; Microglia: immunology (MeSH) ; Microglia: pathology (MeSH) ; Nootropic Agents: administration & dosage (MeSH) ; Obesity: complications (MeSH) ; Obesity: metabolism (MeSH) ; Phagocytosis (MeSH) ; Protein Folding (MeSH) ; Risk Factors (MeSH) ; Severity of Illness Index (MeSH) ; Anti-Inflammatory Agents, Non-Steroidal ; Biomarkers ; Inflammation Mediators ; Nootropic Agents

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Contributing Institute(s):

1. Neuroinflammation, Biomarker (AG Heneka ; AG Heneka)
2. Innate Immunity in Neurodegeneration (AG Latz ; AG Latz)
3. Vascular Neurology (AG Petzold ; AG Petzold)

Research Program(s):

1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)
2. 344 - Clinical and Health Care Research (POF3-344) (POF3-344)

Appears in the scientific report 2015

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Database coverage:
; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; Ebsco Academic Search ; IF >= 25 ; JCR ; NCBI Molecular Biology Database ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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