5 Result(s)
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Ali Mortazavi
Biomedicine
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Article
Open AccessA Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques
The TREM2 R47H variant is one of the strongest genetic risk factors for late-onset Alzheimer’s Disease (AD). Unfortunately, many current Trem2 R47H mouse models are associated with cryptic mRNA splicing of the mu...
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Article
Open AccessC5aR1 antagonism alters microglial polarization and mitigates disease progression in a mouse model of Alzheimer’s disease
Multiple studies have recognized the involvement of the complement cascade during Alzheimer’s disease pathogenesis. However, the specific role of C5a-C5aR1 signaling in the progression of this neurodegenerativ...
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Article
Open AccessModulation of C5a–C5aR1 signaling alters the dynamics of AD progression
The complement system is part of the innate immune system that clears pathogens and cellular debris. In the healthy brain, complement influences neurodevelopment and neurogenesis, synaptic pruning, clearance o...
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Article
Open AccessTranscriptome analysis of heterogeneity in mouse model of metastatic breast cancer
Cancer metastasis is a complex process involving the spread of malignant cells from a primary tumor to distal organs. Understanding this cascade at a mechanistic level could provide critical new insights into ...
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Article
Open AccessPrevention of C5aR1 signaling delays microglial inflammatory polarization, favors clearance pathways and suppresses cognitive loss
Pharmacologic inhibition of C5aR1, a receptor for the complement activation proinflammatory fragment, C5a, suppressed pathology and cognitive deficits in Alzheimer's disease (AD) mouse models. To validate that...
