Abstract
Alzheimer's disease (AD) is the most common form of dementia that mainly affects the cognitive functions of the aged populations. Trigonella foenum-graecum (L.) (fenugreek), a traditionally well utilized medicinal plant ubiquitously used as one of the main food additive worldwide, is known to have numerous beneficial health effects. Fenugreek seed extract could be able to inhibit the activity of acetylcholinesterase (AChE), a key enzyme involved in the pathogenesis of AD, and further shown to have anti-parkinsonic effect. The present study was aimed to explore the neuroprotective effect of fenugreek seed powder (FSP) against aluminium chloride (AlCl3) induced experimental AD model. Administration of germinated FSP (2.5, 5 and 10% mixed with ground standard rat feed) protected AlCl3 induced memory and learning impairments, Al overload, AChE hyperactivity, amyloid β (Aβ) burden and apoptosis via activating Akt/GSK3β pathway. Our present data could confirm the neuroprotective effect of fenugreek seeds. Further these results could lead a possible therapeutics for the management of neurodegenerative diseases including AD in future.
Highlights
Dementia is an enervating disorder, which gradually declines the cognitive functions including memory, language, speech, orientation, judgment and learning capacity[1]
Anti-rabbit-Bax, Bad, Bcl-2, Bcl–xL, cyto-c, pro and cleaved caspases-3,9, GSK-3β, pGSK-3β, pAkt, Voltage-dependent anion channel (VDAC), anti- β actin and horseradish peroxidase (HRP) conjugated goat anti-rabbit IgG were procured from Cell Signaling
fenugreek seed powder (FSP) alone treatment induced non-significant changes in the expression of pAkt, GSK-3β and pGSK-3β compared with the control group. These results indicate that FSP effectively reversed the AlCl3 induced neurotoxicity by augmenting the expressions of pAkt and pGSK3β (Fig 8A, 8B & 8C)
Summary
Dementia is an enervating disorder, which gradually declines the cognitive functions including memory, language, speech, orientation, judgment and learning capacity[1]. AD is accompanied by three main structural changes in the brain including (i) neuronal loss, formation and accumulation of hyperphosphorylated tau protein termed neurofibrillary tangles (NFT) and aggregation of β-amyloid (Aβ) peptides termed senile or amyloid plaques [3]. These changes are most prominent in the cholinergic system, in hippocampus and cortex, which is closely associated with memory loss and cognitive dysfunction in AD[4].
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