Journal Article (Review Article)

DZNE-2025-00587

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

Heneka, M. ; van der Flier, W. M. ; Jessen, F.Extern* ; Hoozemanns, J. ; Thal, D. R. ; Boche, D. ; Brosseron, F.DZNE* ; Teunissen, C. ; Zetterberg, H. ; Jacobs, A. H. ; Edison, P. ; Ramirez, A.Extern* ; Cruchaga, C. ; Lambert, J.-C. ; Laza, A. R. ; Sanchez-Mut, J. V. ; Fischer, A.DZNE* ; Castro-Gomez, M. S.Extern* ; Stein, T. D. ; Kleineidam, L.DZNE* ; Wagner, M.Extern* ; Neher, J. J.DZNE* ; Cunningham, C. ; Singhrao, S. K. ; Prinz, M. ; Glass, C. K. ; Schlachetzki, J. C. M. ; Butovsky, O. ; Kleemann, K. ; De Jaeger, P. L. ; Scheiblich, H. ; Brown, G. C. ; Landreth, G. ; Moutinho, M. ; Grutzendler, J. ; Gomez-Nicola, D. ; McManus, R. M.DZNE* ; Andreasson, K. ; Ising, C. ; Karabag, D. ; Baker, D. J. ; Liddelow, S. A. ; Verkhratsky, A. ; Tansey, M. ; Monsonego, A. ; Aigner, L. ; Dorothée, G. ; Nave, K.-A. ; Simons, M.Extern* ; Constantin, G. ; Rosenzweig, N. ; Pascual, A. ; Petzold, G. C.DZNE* ; Kipnis, J. ; Venegas, C. ; Colonna, M. ; Walter, J. ; Tenner, A. J. ; O'Banion, M. K. ; Steinert, J. R. ; Feinstein, D. L. ; Sastre, M. ; Bhaskar, K. ; Hong, S. ; Schafer, D. P. ; Golde, T. ; Ransohoff, R. M. ; Morgan, D. ; Breitner, J. ; Mancuso, R. ; Riechers, S.-P.

2025
Nature Publ. Group London

This record in other databases:    

Please use a persistent id in citations: doi:10.1038/s41577-024-01104-7

Abstract: Increasing evidence points to a pivotal role of immune processes in the pathogenesis of Alzheimer disease, which is the most prevalent neurodegenerative and dementia-causing disease of our time. Multiple lines of information provided by experimental, epidemiological, neuropathological and genetic studies suggest a pathological role for innate and adaptive immune activation in this disease. Here, we review the cell types and pathological mechanisms involved in disease development as well as the influence of genetics and lifestyle factors. Given the decade-long preclinical stage of Alzheimer disease, these mechanisms and their interactions are driving forces behind the spread and progression of the disease. The identification of treatment opportunities will require a precise understanding of the cells and mechanisms involved as well as a clear definition of their temporal and topographical nature. We will also discuss new therapeutic strategies for targeting neuroinflammation, which are now entering the clinic and showing promise for patients.

Keyword(s): Humans (MeSH) ; Alzheimer Disease: immunology (MeSH) ; Alzheimer Disease: pathology (MeSH) ; Alzheimer Disease: therapy (MeSH) ; Animals (MeSH) ; Neuroinflammatory Diseases: immunology (MeSH) ; Neuroinflammatory Diseases: pathology (MeSH) ; Inflammation: immunology (MeSH) ; Immunity, Innate (MeSH)

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Contributing Institute(s):

1. Neuroinflammation, Biomarker (AG Heneka)
2. Epigenetics and Systems Medicine in Neurodegenerative Diseases (AG Fischer)
3. Neuropsychology (AG Wagner)
4. Neuroimmunology and Neurodegenerative Disease (AG Neher (München))
5. Vascular Neurology (AG Petzold)

Research Program(s):

1. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)
2. 352 - Disease Mechanisms (POF4-352) (POF4-352)

Appears in the scientific report 2025

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Database coverage:
; BIOSIS Previews ; BIOSIS Reviews Reports And Meetings ; Clarivate Analytics Master Journal List ; Current Contents - Clinical Medicine ; Current Contents - Life Sciences ; DEAL Nature ; Ebsco Academic Search ; Essential Science Indicators ; IF >= 90 ; JCR ; Nationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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