PACAP27 mitigates an age-dependent hippocampal vulnerability to PGJ2-induced spatial learning deficits and neuroinflammation in mice.
Jorge A AvilaMagdalena KiprowskaTeneka Jean-LouisPatricia RockwellMaria E Figueiredo-PereiraPeter A SerranoPublished in: Brain and behavior (2019)
Our data show that PGJ2 can produce a retrograde spread of damage not observed in PGJ2-treated young mice, leading to age-dependent neurodegeneration of hippocampal neurons producing learning and memory deficits. PACAP27 can remediate the behavioral and neurodegenerative effects that PGJ2 produces in aged subjects. Targeting specific neurotoxic prostaglandins, such as PGJ2, offers great promise as a new therapeutic strategy downstream of cyclooxygenases, to combat the neuronal deficits induced by chronic inflammation.
Keyphrases
- traumatic brain injury
- cerebral ischemia
- oxidative stress
- high fat diet induced
- big data
- diabetic rats
- climate change
- high glucose
- wild type
- lipopolysaccharide induced
- brain injury
- radiation therapy
- cancer therapy
- middle aged
- machine learning
- cognitive impairment
- metabolic syndrome
- inflammatory response
- adipose tissue
- insulin resistance
- drug delivery