The onset and progression of
Alzheimer's disease (AD) are influenced by a variety of factors. These include oxidative stress, overexpression of
acetylcholinesterase (AChE), depletion of
acetylcholine levels, increased
beta-secretase mediated conversion of
Amyloid Precursor
Protein (APP) to
Amyloid Beta (Abeta), accumulation of Abeta oligomers, decrease in
Brain Derived Neurotrophic factor (
BDNF) and accelerated neuronal apoptosis due to elevated levels of
caspase-3. The currently available therapeutic approaches are inadequate in affecting these
pathological processes except maybe the overexpression of AChE (AChE inhibitors like
donepezil,
rivastigmine). There is an urgent need to develop disease modifying pharmacotherapeutic interventions which have appreciable safety and cost effectiveness. From previously reported in vitro studies and a preliminary assessment of
neuroprotective effect in
scopolamine induced
dementia-like
cognitive impairment in mice,
vanillin has been used as the compound of interest in the present study.
Vanillin, a phytoconstituent, has been used in humans, safely, in the form of a flavouring agent for various foods, beverages, and
cosmetics. Owing to its chemical nature i.e. being a phenolic
aldehyde, it has an additional
antioxidant property that is congruent to the desirable characteristics that are sought in a suitable novel anti-AD agent. In our study,
vanillin proved to have a
nootropic effect in healthy Swiss albino mice as well as an ameliorative effect in
aluminium chloride and
D-galactose induced AD model in mice. Apart from tackling oxidative stress,
vanillin was found to reduce the levels of AChE,
beta secretase,
caspase-3, enhance degradation of Abeta plaques and elevate the levels of
BDNF, in cortical and hippocampal regions.
Vanillin is a promising candidate for being incorporated into the search for safe and effective anti-AD molecules. However, further research might be needed to warrant its application clinically.