Azilsartan prevents central modulation of BDNF and PPARγ in Alzheimer's pathology through amyloidogenic and inflammatory pathways: experimental and computational evidence.
📄 Abstract
Complex progressive neurodegenerative Alzheimer's disease is characterized by cognitive decline, memory impairment, and accumulation of amyloid and tau pathologies, along with aggravation of neuroinflammatory and oxidative stress pathways. In our previous studies, the potential of azilsartan, a widely used angiotensin receptor blocker (ARB), was demonstrated to possess neuroprotective action when administered through intranasal route, improving memory and cognition through modulation of central renin-angiotensin signalling in a demented animal model. With the intranasal administration, azilsartan nanoemulgel offers the ability to bypass the BBB due to the use of the olfactory and trigeminal neural pathways, achieving direct brain targeting of the therapeutics. In the present study, the neuroprotective effect of azilsartan (5 mg/kg via intranasal route consequently for 45 days) was further validated in an AlCl