Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA125103 | ENA |
REPOSITORIES: ENA
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2012-12-21 | E-GEOD-28886 | biostudies-arrayexpress
Project description:Complement protein C1q is induced after injury in the brain and during Alzheimer's disease and has been shown to protect against amyloid-beta induced neuronal death. In this study, we used microarray approach to identify the pathways modulated by C1q that are associated with neuroprotection.
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Project description:We examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease
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Project description:Ehrenstein1997 - The choline-leakage
hypothesis in Alzheimer's disease
This model is described in the article:
The choline-leakage
hypothesis for the loss of acetylcholine in Alzheimer's
disease.
Ehrenstein G, Galdzicki Z, Lange
GD.
Biophys. J. 1997 Sep; 73(3):
1276-1280
Abstract:
We present a hypothesis for the loss of acetylcholine in
Alzheimer's disease that is based on two recent experimental
results: that beta-amyloid causes leakage of choline across
cell membranes and that decreased production of acetylcholine
increases the production of beta-amyloid. According to the
hypothesis, an increase in beta-amyloid concentration caused by
proteolysis of the amyloid precursor protein results in an
increase in the leakage of choline out of cells. This leads to
a reduction in intracellular choline concentration and hence a
reduction in acetylcholine production. The reduction in
acetylcholine production, in turn, causes an increase in the
concentration of beta-amyloid. The resultant positive feedback
between decreased acetylcholine and increased beta-amyloid
accelerates the loss of acetylcholine. We compare the
predictions of the choline-leakage hypothesis with a number of
experimental observations. We also approximate it with a pair
of ordinary differential equations. The solutions of these
equations indicate that the loss of acetylcholine is very
sensitive to the initial rate of beta-amyloid production.
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2024-09-02 | BIOMD0000000553 | BioModels
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
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