Abstract
In recent years, ongoing interest in ischemic brain injury research has provided data showing that ischemic episodes are involved in the development of Alzheimer’s disease-like neuropathology. Brain ischemia is the second naturally occurring neuropathology, such as Alzheimer’s disease, which causes the death of neurons in the CA1 region of the hippocampus. In addition, brain ischemia was considered the most effective predictor of the development of full-blown dementia of Alzheimer’s disease phenotype with a debilitating effect on the patient. Recent knowledge on the activation of Alzheimer’s disease-related genes and proteins—e.g., amyloid protein precursor and tau protein—as well as brain ischemia and Alzheimer’s disease neuropathology indicate that similar processes contribute to neuronal death and disintegration of brain tissue in both disorders. Although brain ischemia is one of the main causes of death in the world, there is no effective therapy to improve the structural and functional outcomes of this disorder. In this review, we consider the promising role of the protective action of curcumin after ischemic brain injury. Studies of the pharmacological properties of curcumin after brain ischemia have shown that curcumin has several therapeutic properties that include anti-excitotoxic, anti-oxidant, anti-apoptotic, anti-hyperhomocysteinemia and anti-inflammatory effects, mitochondrial protection, as well as increasing neuronal lifespan and promoting neurogenesis. In addition, curcumin also exerts anti-amyloidogenic effects and affects the brain’s tau protein. These results suggest that curcumin may be able to serve as a potential preventive and therapeutic agent in neurodegenerative brain disorders.
Highlights
Brain ischemic injury in humans is the third cause of disability and the second cause of death, which may soon become the leading cause of full-blown dementia of Alzheimer’s disease type [1,2,3,4,5,6,7,8,9]
The microtubule-associated tau protein is hypophosphorylated in the ischemic brains of patients and in experimental cerebral ischemia and generates intraneuronal neurofibrillary tangles and/or neurofibrillary tangle-like tauopathy that are a key in the ongoing neuropathology of Alzheimer’s disease [35,83]
Embryonic stem cell exosomes loaded with curcumin restored the neurovascular unit after ischemic brain injury [112,113]. These results suggest that combining exosomal potentials from embryonic stem cells with curcumin may help restore the neurovascular unit after ischemic brain injury in mice
Summary
Brain ischemic injury in humans is the third cause of disability and the second cause of death, which may soon become the leading cause of full-blown dementia of Alzheimer’s disease type [1,2,3,4,5,6,7,8,9]. Due to the lack of translation of experimental neuroprotective agents for use in clinical conditions [41], we have focused our attention on improving functional outcomes after ischemia, instead of protecting neurons during ischemic damage To this end, we should improve the function of persistent neurons after ischemia [14,16], and new therapies should be designed to reverse synaptic plasticity deficits to improve the functional outcome after brain ischemia, effectively extending the therapeutic window. Post-ischemic brain damage is undoubtedly one of the most common multifactorial forms of neurodegeneration, including a series of abnormal cell/molecular processes taking place at different times during recirculation and progressively various areas of the brain It seems that ischemic episodes favor the development of Alzheimer’s disease-like neurodegeneration through numerous mechanisms including neuronal loss, synaptic dysfunction, neuroinflammation, accumulation of various parts of the amyloid protein precursor, tau protein dysfunction and dysregulation of Alzheimer’s disease-related genes, white matter lesions, and general brain atrophy. The progress in understanding the key processes of brain ischemia-induced changes of the Alzheimer’s disease phenotype and genotype will help to develop the prevention and treatment strategies against neurodegeneration and dementia generated by ischemia
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