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000284351 1001_ $$0P:(DE-2719)9001455$$aCangalaya, Carla$$b0$$eFirst author$$udzne
000284351 245__ $$aCerebellar Resistance to Amyloid Plaque Deposition and Elevated Microglial ECM Proteoglycan Uptake in 5xFAD Mice.
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000284351 520__ $$aIn both Alzheimer's disease (AD) patients and animal models, senile plaques are generally observed in the cerebral cortex rather than the cerebellum. The mechanisms underlying the regional resistance of the cerebellum to amyloid plaque deposition remain poorly understood. We investigated this cerebellar resistance using 5xFAD mice, an amyloidosis model with high expression of mutant human APP and PSEN1 in the cortex and cerebellum. In aged 5xFAD mice, the cerebellum had minimal amyloid-β (Aβ) deposition despite robust transgene expression, correlating with lower expression levels of IBA1, CD68, TREM2, and CD36 (although elevated expression of CD45 and MHC I) compared to the cortex. Consistent with the absence of plaques, cerebellar tissue lacked the dystrophic VGLUT1-positive synaptic accumulations prominent in the cortex. Cerebellar microglia maintained a distinct, less inflammatory phenotype yet displayed efficient clearance activity. Notably, ASC inflammasome specks-capable of seeding Aβ aggregation-were paradoxically more abundant in the cerebellum, implying that rapid Aβ clearance prevents these seeds from driving plaque formation. Furthermore, key extracellular matrix (ECM) proteoglycans brevican and aggrecan were elevated in the 5xFAD cerebellum. Cerebellar microglia showed enhanced internalization of brevican alongside small Aβ aggregates, exceeding that in cortical microglia. These findings indicate that region-specific microglial and ECM interactions-particularly efficient uptake and degradation of ECM-Aβ co-aggregates-may underlie the cerebellum's resilience to amyloid plaque pathology.
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000284351 650_7 $$2Other$$aAlzheimer’s disease
000284351 650_7 $$2Other$$acerebellum
000284351 650_7 $$2Other$$acortex
000284351 650_7 $$2Other$$aextracellular matrix
000284351 650_7 $$2Other$$amicroglia
000284351 650_7 $$2Other$$aperineuronal nets
000284351 650_7 $$2Other$$aproteoglycans
000284351 650_7 $$2Other$$asynaptic pruning
000284351 650_7 $$2NLM Chemicals$$aProteoglycans
000284351 650_7 $$2NLM Chemicals$$aAmyloid beta-Peptides
000284351 650_2 $$2MeSH$$aAnimals
000284351 650_2 $$2MeSH$$aMicroglia: metabolism
000284351 650_2 $$2MeSH$$aMicroglia: pathology
000284351 650_2 $$2MeSH$$aPlaque, Amyloid: metabolism
000284351 650_2 $$2MeSH$$aPlaque, Amyloid: pathology
000284351 650_2 $$2MeSH$$aCerebellum: metabolism
000284351 650_2 $$2MeSH$$aCerebellum: pathology
000284351 650_2 $$2MeSH$$aMice, Transgenic
000284351 650_2 $$2MeSH$$aMice
000284351 650_2 $$2MeSH$$aAlzheimer Disease: pathology
000284351 650_2 $$2MeSH$$aAlzheimer Disease: metabolism
000284351 650_2 $$2MeSH$$aExtracellular Matrix: metabolism
000284351 650_2 $$2MeSH$$aProteoglycans: metabolism
000284351 650_2 $$2MeSH$$aDisease Models, Animal
000284351 650_2 $$2MeSH$$aHumans
000284351 650_2 $$2MeSH$$aAmyloid beta-Peptides: metabolism
000284351 650_2 $$2MeSH$$aCerebral Cortex: metabolism
000284351 650_2 $$2MeSH$$aCerebral Cortex: pathology
000284351 7001_ $$aDüsedau, Henning Peter$$b1
000284351 7001_ $$aDunay, Ildiko Rita$$b2
000284351 7001_ $$0P:(DE-2719)2810577$$aDityatev, Alexander$$b3
000284351 7001_ $$0P:(DE-2719)2809920$$aStoyanov, Stoyan Borislavov$$b4$$eLast author
000284351 770__ $$aTargeting Cellular Microenvironment in Aging and Disease
000284351 773__ $$0PERI:(DE-600)2661518-6$$a10.3390/cells15020182$$gVol. 15, no. 2, p. 182 -$$n2$$p182$$tCells$$v15$$x2073-4409$$y2026
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