% IMPORTANT: The following is UTF-8 encoded. This means that in the presence % of non-ASCII characters, it will not work with BibTeX 0.99 or older. % Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or % “biber”. @ARTICLE{Heneka:278101, author = {Heneka, Michael and van der Flier, Wiesje M and Jessen, Frank and Hoozemanns, Jeroen and Thal, Dietmar Rudolf and Boche, Delphine and Brosseron, Frederic and Teunissen, Charlotte and Zetterberg, Henrik and Jacobs, Andreas H and Edison, Paul and Ramirez, Alfredo and Cruchaga, Carlos and Lambert, Jean-Charles and Laza, Agustin Ruiz and Sanchez-Mut, Jose Vicente and Fischer, Andre and Castro-Gomez, Mario Sergio and Stein, Thor D and Kleineidam, Luca and Wagner, Michael and Neher, Jonas J and Cunningham, Colm and Singhrao, Sim K and Prinz, Marco and Glass, Christopher K and Schlachetzki, Johannes C M and Butovsky, Oleg and Kleemann, Kilian and De Jaeger, Philip L and Scheiblich, Hannah and Brown, Guy C and Landreth, Gary and Moutinho, Miguel and Grutzendler, Jaime and Gomez-Nicola, Diego and McManus, Róisín M and Andreasson, Katrin and Ising, Christina and Karabag, Deniz and Baker, Darren J and Liddelow, Shane A and Verkhratsky, Alexei and Tansey, Malu and Monsonego, Alon and Aigner, Ludwig and Dorothée, Guillaume and Nave, Klaus-Armin and Simons, Mikael and Constantin, Gabriela and Rosenzweig, Neta and Pascual, Alberto and Petzold, Gabor C and Kipnis, Jonathan and Venegas, Carmen and Colonna, Marco and Walter, Jochen and Tenner, Andrea J and O'Banion, M Kerry and Steinert, Joern R and Feinstein, Douglas L and Sastre, Magdalena and Bhaskar, Kiran and Hong, Soyon and Schafer, Dorothy P and Golde, Todd and Ransohoff, Richard M and Morgan, David and Breitner, John and Mancuso, Renzo and Riechers, Sean-Patrick}, title = {{N}euroinflammation in {A}lzheimer disease.}, journal = {Nature reviews / Immunology}, volume = {25}, number = {5}, issn = {1474-1733}, address = {London}, publisher = {Nature Publ. Group}, reportid = {DZNE-2025-00587}, pages = {321 - 352}, year = {2025}, 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.}, subtyp = {Review Article}, keywords = {Humans / Alzheimer Disease: immunology / Alzheimer Disease: pathology / Alzheimer Disease: therapy / Animals / Neuroinflammatory Diseases: immunology / Neuroinflammatory Diseases: pathology / Inflammation: immunology / Immunity, Innate}, cin = {AG Heneka / AG Fischer / AG Wagner / AG Neher (München) / AG Petzold}, ddc = {570}, cid = {I:(DE-2719)1011303 / I:(DE-2719)1410002 / I:(DE-2719)1011201 / I:(DE-2719)1110011 / I:(DE-2719)1013020}, pnm = {353 - Clinical and Health Care Research (POF4-353) / 352 - Disease Mechanisms (POF4-352)}, pid = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-352}, typ = {PUB:(DE-HGF)16}, pubmed = {pmid:39653749}, doi = {10.1038/s41577-024-01104-7}, url = {https://pub.dzne.de/record/278101}, }