GM2 ganglioside accumulation causes neuroinflammation and behavioral alterations in a mouse model of early onset Tay-Sachs disease.
Seçil Akyıldız DemirZehra Kevser TimurNurselin AteşLuis Alarcón MartínezVolkan SeyrantepePublished in: Journal of neuroinflammation (2020)
Altogether, our data suggest that Hexa-/-Neu3-/- mice display a phenotype similar to Tay-Sachs patients suffering from chronic neuroinflammation triggered by GM2 accumulation. Furthermore, our work contributes to better understanding of the neuropathology in a mouse model of early onset Tay-Sachs disease.
Keyphrases
- early onset
- mouse model
- late onset
- end stage renal disease
- traumatic brain injury
- lipopolysaccharide induced
- ejection fraction
- chronic kidney disease
- newly diagnosed
- lps induced
- cognitive impairment
- prognostic factors
- type diabetes
- metabolic syndrome
- inflammatory response
- big data
- adipose tissue
- cerebral ischemia
- insulin resistance
- patient reported outcomes
- high fat diet induced
- brain injury