% 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},
}