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http://dspace.bits-pilani.ac.in:8080/jspui/handle/123456789/13413Full metadata record
| DC Field | Value | Language |
|---|---|---|
| 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 |
| Appears in Collections: | Department of Pharmacy | |
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