Abstract
For thousands of years, mankind has been using plant extracts or plants themselves as medicinal herbs. Currently, there is a great deal of public interest in naturally occurring medicinal substances that are virtually non-toxic, readily available, and have an impact on well-being and health. It has been noted that dietary curcumin is one of the regulators that may positively influence changes in the brain after ischemia. Curcumin is a natural polyphenolic compound with pleiotropic biological properties. The observed death of pyramidal neurons in the CA1 region of the hippocampus and its atrophy are considered to be typical changes for post-ischemic brain neurodegeneration and for Alzheimer’s disease. Additionally, it has been shown that one of the potential mechanisms of severe neuronal death is the accumulation of neurotoxic amyloid and dysfunctional tau protein after cerebral ischemia. Post-ischemic studies of human and animal brains have shown the presence of amyloid plaques and neurofibrillary tangles. The significant therapeutic feature of curcumin is that it can affect the aging-related cellular proteins, i.e., amyloid and tau protein, preventing their aggregation and insolubility after ischemia. Curcumin also decreases the neurotoxicity of amyloid and tau protein by affecting their structure. Studies in animal models of cerebral ischemia have shown that curcumin reduces infarct volume, brain edema, blood-brain barrier permeability, apoptosis, neuroinflammation, glutamate neurotoxicity, inhibits autophagy and oxidative stress, and improves neurological and behavioral deficits. The available data suggest that curcumin may be a new therapeutic substance in both regenerative medicine and the treatment of neurodegenerative disorders such as post-ischemic neurodegeneration.
Highlights
Today ischemic stroke is a huge and growing health challenge in the world
It is well known that post-ischemic brain neurodegeneration is caused by a set of genetic and proteomic changes that lead to neuronal death in an amyloid- and tau protein-dependent manner, with progressive inflammation resulting in brain atrophy with the development of full-blown Alzheimer’s disease dementia [4,10,11]
Injury and death of neuronal cells, with the accumulation of diffuse amyloid and senile plaques, the development of neurofibrillary tangles, as well as neurological deficits with the development of full-blown dementia are the main phenomena in post-ischemic brain neurodegeneration in animals and humans
Summary
Today ischemic stroke is a huge and growing health challenge in the world. In developed and developing countries, post-ischemic brain neurodegeneration is becoming more common in view of the progressive aging of the world’s population. It is well known that post-ischemic brain neurodegeneration is caused by a set of genetic and proteomic changes that lead to neuronal death in an amyloid- and tau protein-dependent manner, with progressive inflammation resulting in brain atrophy with the development of full-blown Alzheimer’s disease dementia [4,10,11]. Research indicates that hyperphosphorylation of the tau protein with the final formation of neurofibrillary tangles plays a key role in the development of post-ischemic brain neurodegeneration as in Alzheimer’s disease [35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54]. This work focuses on the neuroprotective effects of curcumin’s pleiotropic properties on the ischemic brain
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