Alzheimer's disease (AD) is a neurodegenerative brain disorder that progressively impairs long-term and working memory. The function and mechanism of PA(Patchouli alcohol) in improving AD in the external treatment of encephalopathy remain unclear. This study aimed to investigate the therapeutic effect of PA on AD using an Aβ 1-42 induced AD mouse model with LPS(Lipopolysaccharide) stimulation of BV2 microglial cells. Additionally, we aimed to explore the potential mechanism of PA in enhancing autophagy and reducing neuroinflammation through the AMPK (AMP-activated protein kinase)/mTOR (Mammaliam target of rapamycin) signaling pathway. The Morris water maze was used to assess cognitive function, and cortical and hippocampal tissues were collected for further analysis of the corresponding signaling pathways and inflammatory changes through biological experiments. Our research findings demonstrate that PA has a significant positive impact on cognitive and memory impairments in mice that have been induced with Aβ 1-42 -induced AD. Additionally, PA was also found to revert the activation of microglia induced by LPS. These effects may be attributed to the reduction of neuroinflammation and enhancement of the AMPK/mTOR autophagy pathway. Therefore, PA may serve as an effective therapeutic option to prevent or delay the progression of AD-associated memory dysfunction.
Keyphrases
- working memory
- signaling pathway
- protein kinase
- inflammatory response
- lps induced
- lipopolysaccharide induced
- oxidative stress
- diabetic rats
- induced apoptosis
- high glucose
- mouse model
- cell proliferation
- skeletal muscle
- cell death
- cerebral ischemia
- traumatic brain injury
- pi k akt
- epithelial mesenchymal transition
- gene expression
- drug induced
- type diabetes
- transcranial direct current stimulation
- endothelial cells
- attention deficit hyperactivity disorder
- toll like receptor
- spinal cord injury
- multiple sclerosis
- immune response
- cognitive impairment
- adipose tissue
- mild cognitive impairment
- blood brain barrier
- replacement therapy