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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Background: Animal models of amyloidosis have been instrumental in Alzheimer's disease (AD) research since they can resemble pathophysiological features of human AD. Nevertheless, each model is generated through different genetic engineering strategies, resulting in distinct phenotypes. In this context, whether AD core molecular programs are conserved among mouse models remains to be addressed.
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Alzheimers Dement
December 2024
Janssen Research & Development, A Division of Janssen Pharmaceutica, Beerse, Belgium, Beerse, Belgium.
Background: Microglial cells have emerged as key players in the pathogenesis of Alzheimer's disease (AD). They act as a first line defense and fulfil a crucial role during brain development and circuit homeostasis. Microglia are involved in the removal of debris, control neural activity, regulate synaptic plasticity, and synapse pruning.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Stark Neurosciences Research Institute, Indiana University School of Medicine, Indianapolis, IN, USA.
Background: Alzheimer's disease (AD) is a complex, multifactorial pathology with high heterogeneity in biological alterations. Our understanding of cellular and molecular mechanisms from disease risk variants to various phenotypes is still limited. Mouse models of AD serve as indispensable platforms for comprehensively characterizing AD pathology, disease progression, and biological mechanisms.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
Background: Replacement, Reduction, and Refinement (3R) guidelines propose the use of alternative models to study human diseases. These models have high homology and are less onerous compared to rodents, which dominate Alzheimer's disease (AD) research. However, it is still necessary to investigate whether evolutionary components are conserved among AD models cross-species.
View Article and Find Full Text PDFBasic Science and Pathogenesis.
Alzheimers Dement
December 2024
Sanders-Brown Center on Aging, Lexington, KY, USA.
Background: Compared to the 'neutral' E3, the E4 allele of Apolipoprotein E (APOE) confers up to a 15-fold increase in Alzheimer's Disease (AD) risk. Conversely, the neuroprotective E2 allele decreases AD risk by a similar degree. Here, we aimed to assess the therapeutic potential of cell-type specific allelic 'switching' by investigating the physiological and neuropathological changes associated with an inducible, in vivo APOE4 to APOE2 transition in astrocytes using a novel transgenic mouse model METHOD: The APOE "switch mouse" (APOE4s2) uses the Cre-loxP system to allow for inducible APOE allele switching from E4 to E2.
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