Berberine is one of the most important quinoline alkaloids, which has shown numerous pharmacological activities. There are pieces of evidence that berberine serves as a promising substance for treating Alzheimer's disease (AD). Recently, numerous studies on animal models have shown the neuroprotective role of berberine. AD is a complex disease having multiple pathological factors. Berberine restrains the deposition of amyloid plaques and neurofibrillary tangles. Substantial studies have demonstrated that berberine may also exhibit the protective effect against the risk factors associated with AD. This review illustrates the role of berberine in neuroinflammation, oxidative stress and its activity against acetylcholinesterase enzyme. It also focuses on the bioavailability and safety of berberine in AD. However, more investigations are required to explore the bioavailability and safety assessment of berberine and its new perspectives in limiting the AD-related pathogenesis and risk factors. Practical applicationsCurrent therapeutic measures only provide symptomatic relief against AD by slowing memory loss, resolving thinking problems and behavioral issues. In recent past years, many biological actions and potential therapeutic applications have been observed by berberine particularly in neurological diseases. Berberine has been investigated by various researchers for its activity against AD. This review demonstrates a variety of mechanisms by which berberine imparts its neuroprotective roles and provides the possible mechanism of action of berberine by which it prevents the formation of neurofibrillary tangles and disaggregation of amyloid beta plaques in AD. It also focuses that berberine limits the neuroinflammation and oxidative stress in AD. Preclinical aspects of berberine against AD are also discussed. Eventually, a prospect is formulated that berberine might be a therapeutically significant agent for treating and preventing AD.

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Alzheimer's disease (AD) is a progressive and frequent neurodegenerative disease in elderly people. In the 21st century, owing to the increasing prevalence of AD, there is a crucial need for finding better and more effective pharmacotherapeutic approaches. This review article demonstrated various sources and possible metabolic pathways of curcuminoids obtained from Curcuma longa herb, to prevent and treat AD, but the information related to the metabolic fate of curcuminoids is deficient. Different in vitro and in vivo research studies demonstrating the mechanisms by which curcuminoids attenuated AD have been summarized. Administration of curcuminoids has been indicated to inhibit hyperphosphorylation of tau protein, deposition, and oligomerization of amyloid beta plaques in several AD models. Curcuminoids also inhibit acetylcholinesterase activity, chelate metals and form complexes, have antioxidant properties, mediate neuroinflammatory signaling pathways by altering the activity of microglial cells, and modulate other related signaling pathways such as the heme-oxygenase pathway and the insulin signaling pathways. Briefly curcuminoids exhibit the capability to be more productive and efficacious compared to many recent treatments due to their antioxidant, delayed neuron degeneration, and anti-inflammatory potential. Although their effectiveness as a curative agent is considered to be reduced due to their low bioavailability, if the issue of curcuminoids' low bioavailability is resolved then curcuminoid-based medications are hopefully on the horizon against AD.