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LRRK2 deficiency mitigates amyloid β deposition-mediated pathology in a murine Alzheimer’s disease model by reprogramming microglia
LRRK2 deficiency may reduce amyloid beta-related damage in a mouse Alzheimer's model by changing immune brain cells
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Abstract
5xFAD; mice exhibited improved learning and memory compared to .
- LRRK2 deficiency is associated with reduced Aβ plaque accumulation in the brains of AD mice.
- Decreased microglial and astrocytic presence was observed within the central region of Aβ plaques in LRRK2 mice.
- A reduction in proinflammatory cytokines and changes in microglial phenotype were noted in the absence of LRRK2.
- Synaptic loss was prevented in 5xFAD;LRRK2 mice, restoring the balance between excitatory and inhibitory synapses.
- Enhanced microglial phagocytosis in LRRK2-deficient mice contributed to decreased Aβ aggregation and glial activation.
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Key numbers
14 of 17
Cognitive Improvement
Mice showing improved performance in the Morris water maze test.
5 of 5
Plaque Reduction
Mice with deficiency exhibited reduced amyloid β plaques.