Home > Publications Database > Decoding transcriptional regulation of microglia associated with amyloid plaques > print

001     283066
005     20251230103620.0
024 7 _ |a 10.1002/alz70855_106751
|2 doi
024 7 _ |a pmid:41447077
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024 7 _ |a 1552-5260
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024 7 _ |a 1552-5279
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037 _ _ |a DZNE-2025-01473
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Schlachetzki, Johannes C M
|b 0
111 2 _ |a Alzheimer’s Association International Conference
|g AAIC 25
|c Toronto
|d 2025-07-27 - 2025-07-31
|w Canada
245 _ _ |a Decoding transcriptional regulation of microglia associated with amyloid plaques
260 _ _ |c 2025
336 7 _ |a Abstract
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336 7 _ |a Conference Paper
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520 _ _ |a Beyond the progressive accumulation of amyloid-beta and hyperphosphorylated tau, Alzheimer's disease (AD) is accompanied by phenotypic changes in microglia, the innate immune cells of the brain. In particular, microglia in the vicinity of Amyloid-plaques, also known as MGnD or DAM, are defined by distinct changes in their gene expression signature, e.g., upregulation of Trem2 mRNA. However, the precise transcriptional mechanism that drives microglia phenotype in response to amyloid is not defined.Here, we isolated microglia from the APP/PS1 transgenic mouse model followed by ATAC-seq.We provide evidence for a model in which differential activation of a common set of transcriptional regulators that includes members of the MITF/TFE, AP-1 and EGR transcription factor families drives the amyloid-plaque associated microglia phenotype.Collectively, these findings reveal the framework of the transcriptional circuitry that is used to establish a range of neurodegenerative pathology-associated microglia phenotypes.
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650 _ 7 |a Amyloid beta-Protein Precursor
|2 NLM Chemicals
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 7 |a Presenilin-1
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Microglia: metabolism
|2 MeSH
650 _ 2 |a Microglia: pathology
|2 MeSH
650 _ 2 |a Mice, Transgenic
|2 MeSH
650 _ 2 |a Alzheimer Disease: pathology
|2 MeSH
650 _ 2 |a Alzheimer Disease: genetics
|2 MeSH
650 _ 2 |a Alzheimer Disease: metabolism
|2 MeSH
650 _ 2 |a Mice
|2 MeSH
650 _ 2 |a Disease Models, Animal
|2 MeSH
650 _ 2 |a Plaque, Amyloid: pathology
|2 MeSH
650 _ 2 |a Plaque, Amyloid: metabolism
|2 MeSH
650 _ 2 |a Brain: pathology
|2 MeSH
650 _ 2 |a Brain: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Protein Precursor: genetics
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Presenilin-1: genetics
|2 MeSH
700 1 _ |a Zhou, Yi
|0 P:(DE-HGF)0
|b 1
700 1 _ |a Spann, Nathan
|b 2
700 1 _ |a Kleemann, Kilian Leon
|b 3
700 1 _ |a McManus, Roisin M
|0 P:(DE-2719)2811671
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|u dzne
700 1 _ |a Heneka, Michael T
|b 5
700 1 _ |a Butovsky, Oleg
|b 6
700 1 _ |a Glass, Christopher K
|b 7
773 _ _ |a 10.1002/alz70855_106751
|g Vol. 21 Suppl 1, no. Suppl 1, p. e106751
|0 PERI:(DE-600)2201940-6
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|t Alzheimer's and dementia
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|y 2025
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856 4 _ |y OpenAccess
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910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
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