| dc.contributor.author |
Taliyan, Rajeev |
|
| dc.date.accessioned |
2023-12-14T04:01:44Z |
|
| dc.date.available |
2023-12-14T04:01:44Z |
|
| dc.date.issued |
2021-12 |
|
| dc.identifier.uri |
https://alz-journals.onlinelibrary.wiley.com/doi/abs/10.1002/alz.058695 |
|
| dc.identifier.uri |
http://dspace.bits-pilani.ac.in:8080/xmlui/handle/123456789/13413 |
|
| dc.description.abstract |
Alzheimer's disease (AD) is a multifactorial neurodegenerative condition and the most common cause of its initiation is accumulation of oligomeric amyloid beta1-42 (Aβ1-42). In recent past, several studies have shown autophagy deficits in AD may resulted accumulation of misfolded protein, Aβ1-42 and phosphorylated tau (ptau). Fibroblast growth factor 21 (FGF21), a metabolic hormone, has shown strong neuroprotective efficacy via increasing autophagic flux in AD. Therefore, this study was designed to investigate the synergistic neuroprotective efficacy of lentiviral FGF21 gene (LV-FGF21) delivery and rapamycin-autophagy modulator in Aβ1-42 induced AD in rats. |
en_US |
| dc.language.iso |
en |
en_US |
| dc.publisher |
Wiley |
en_US |
| dc.subject |
Pharmacy |
en_US |
| dc.subject |
Alzheimer's disease (AD) |
en_US |
| dc.subject |
Neurodegenerative condition |
en_US |
| dc.title |
Fibroblast Growth Factor 21 and Autophagy Modulation Ameliorates Amyloid β-Induced Alzheimer Disease Pathology in Rats |
en_US |
| dc.type |
Article |
en_US |