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The dopamine analogue CA140 alleviates AD pathology, neuroinflammation, and rescues synaptic/cognitive functions by modulating DRD1 signaling or directly binding to Abeta
The dopamine-like drug CA140 may reduce Alzheimer's signs, brain inflammation, and memory problems by affecting dopamine signals or directly interacting with harmful brain proteins
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Abstract
CA140 treatment significantly reduced Aβ/tau fibrillation and neuroinflammation in aged 5xFAD mice, a model of Alzheimer's disease.
- CA140 treatment lowered the number of Aβ plaques and tau hyperphosphorylation in aged 5xFAD mice.
- The treatment inhibited NLRP3 activation, which is associated with neuroinflammation.
- CA140 downregulated the expression of cxcl10 and c1qa, markers of reactive astrocytes and their interaction with disease-associated microglia.
- In primary microglial cells, CA140 increased markers of homeostatic microglia and decreased markers associated with proliferative and lipid-droplet-accumulating microglia.
- CA140 treatment improved long-term memory and dendritic spine number while reversing impairments in long-term potentiation caused by scopolamine.
- The observed effects on cognitive and synaptic function were linked to dopamine D1 receptor signaling.
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Key numbers
30 mg/kg
Decrease in Aβ Plaques
Aged 5xFAD mice treated with CA140 daily for 14 days.
30 mg/kg
Increase in Dendritic Spine Number
Dendritic spine density measured after CA140 treatment in 5xFAD mice.
30 mg/kg
Long-term Memory Improvement
Cognitive function assessed after CA140 administration in 5xFAD mice.