Alzheimer's disease (AD) is a brain disorder that usually has a chronic or
progressive nature and results in a reduction in cognitive function that is more than
what would be expected from the typical effects of the biological aging process, which
is a significant cause of dementia. Even though tau and amyloid-β (Aβ) have been
identified as the main components in the formation of tangles and plaques,
respectively, there is still little known about the causes of Alzheimer’s disease, and no
effective treatments are available. It affects an estimated 40 million people worldwide,
most of whom are over 60, and is expected to double every 20 years, at least until
2050. Most current efforts at therapeutic intervention are based on the hypothesized
pathogenic mechanisms for AD. These include amyloids, inflammatory mediators,
excitotoxicity, steroid hormone deficiencies, loss of cholinergic function, dietary factors, oxidative stress, band g-secretase effectors, etc. Still, these therapies were neither
completely effective nor safe for prolonged usage to check this problem. Various
natural products have been tested. One such natural product is andrographolide (AG),
which has several potential therapeutic benefits, including anti-inflammatory,
immunomodulatory, and antiangiogenic properties. It is traditionally used for the
treatment of various ailments. AG and its derivatives were found to be effective in the
reduction of synaptic proteins associated with Alzheimer's disease by overturning the
microglia-mediated growth of pro-inflammatory cytokines, and the research has shown
that these compounds decrease amyloid beta aggregation and suppress the neuroinflammatory response and synaptic dysfunction. In the current review, the therapeutic
potential of andrographolide and its analogs is outlined, and its mechanism of action
against this disease is examined to explore the possibility of AG for the prevention and
treatment of AD.
Keywords: Alzheimer's disease, Andrographolide, Amyloid beta, Dementia, Neurodegenerative disorder.