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Neurodegeneration refers to a condition of neuronal death occurring as a result of progressive disease of long-term and is becoming a major health problem in the 21st century. Neurons degenerated are not replaced resulting in a cognitive loss, many neurodegenerative disorders, such as schizophrenia, depression, Alzheimer's disease (AD), dementia, cerebrovascular impairment, seizure disorders, head injury, parkinsonism. The common pathology of neurodegeneration includes deposition of misfolded proteins such as amyloid-β (Aβ) in Alzheimer's disease, α-synuclein in Parkinson's disease (PD), transactive response DNA-binding protein 43 (TDP-43) in dementia. Neuroprotection refers to the strategies and possible mechanisms that are able to protect the central nervous system (CNS) against neuronal injury and neurodegenerative disorders. The past decade has witnessed an intense interest in herbal plants having long-term health-promoting or medicinal qualities. Comprehensive research and discovery have demonstrated that natural products, medicinal herbs, plant extracts, and their metabolites, have great potential as the neuroprotective agent. Although the precise mechanisms of action of herbal drugs have yet to be determined, some of them have been shown to prevent formation of betaamyloid plaques, promote nerve growth, some inhibit acetylcholinesterase (AChE) enzyme and malondialdehyde (MDA) formation in brain while other exhibits antioxidant activity by increasing the level of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx). Thus the herbal plants can be a valuable source of the drug against neurodegenerative disorders which will require high-throughput screening. This review will highlight the role of herbal plants and their phytoconstituents against neurodegenerative diseases and other related disorders, focusing on their mechanism of action and therapeutic potential.

Preclinical and clinical studies indicated involvement of the central renin-angiotensin system (RAS) in memory functions. However, the role of central angiotensin-converting enzyme (ACE) in memory function is still unclear. The present study investigated the involvement of central ACE in colchicine-induced memory impairment in the context of cholinergic function and oxidative stress. Memory impairment was induced by intracerebral colchicine administration in mice. The ACE inhibitor, perindopril (0.05 and 0.1 mg/kg/day), was administered orally for 14 days. Memory function was evaluated by the Morris water maze (MWM) test from the 14th day on after colchicine injection. Donepezil was used as a standard. Parameters of oxidative stress and cholinergic function, ACE activity in serum and the brain were estimated after the completion of behavioral studies. Colchicine caused memory impairment as revealed by no significant change in latency to reach a hidden platform in the MWM test. Furthermore, there was a significant increase in MDA, ROS, and nitrite levels with a reduction in GSH level and acetylcholinesterase (AChE) activity in the brain of colchicine-treated mice. Colchicine significantly increased brain ACE activity without affecting serum ACE. Donepezil prevented colchicine-induced memory impairment in mice. The antidementic effect of perindopril may be attributed to reduced oxidative stress and improvement in cholinergic function. Moreover, the elevated brain ACE activity was also inhibited by perindopril. The study showed that central ACE plays an important role in colchicine-induced memory deficit, corroborating a number of studies that show that treatment with ACE inhibitors could be neuroprotective.