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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.

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Objective: We sought to investigate the protective activity of candesartan against memory impairment, oxidative stress and cholinergic dysfunction induced by activation of the central renin-angiotensin system. Methods:Male Swiss albino mice were divided into eight groups. Group 1 received vehicle (1.0% w/v gum acacia), orally for 14 d. Learning and memory behavior was assessed by using morris water maze. Biochemical parameters of oxidative stress and cholinergic function were estimated in the brain on day 18. Parameters of oxidative stress and cholinergic function were estimated after the completion of behavioral studies Results: Treatment with a higher dose of colchicines (3µg/mice) caused memory deficit as shown by no significant decrease in escape latency time throughout all the sessions. Results of biochemical estimation showed a marked increase in malondialdehyde (MDA), nitrite level, reduced glutathione (GSH) level, cholinotoxic effect of colchicines has been correlated by marked decrease in acetyl cholinesterase (AChE) activity. Colchicine in a dose of 3 µg/mice has been validated. Pretreatment with candesartan in doses 0.05 and 0.1 mg/kg reverses oxidative stress which can be measured by decreased MDA, nitrite level and increased GSH level. Increased AChE activity may imply protection of cholinergic neurons hence improvement in learning and memory behavior. Conclusion:Preventive treatment with angiotensins receptor blocker, candesartan showed that memory impairment induced by colchicines may be mediated by alteration of central rennin angiotensins system and loss of cholinergic neurons. This study highlighted a number of clinical findings which support marked neuroprotection by blocked of the central AT1 receptor.

Background: Lornoxicam is widely used for its anti-inflammatory, analgesic and antipyretic properties. However, it suffers from the limitations of possessing a relatively short elimination half-life ranging from 3 to 5 h, thereby; leading to repeated dosing which in turn may cause local irritation and ulceration. In addition, LXM also exhibits pHdependent solubility. Effective management of inflammation in diseases such as arthritis requires the formulation of delivery systems that may be able to provide immediate release of drug for instant relief which shall be maintained for a prolonged period. Objective: The present research work was aimed to modify the release pattern of poorly water-soluble drug Lornoxicam by designing a biphasic tablet comprising of solid dispersion (immediate release form) and microspheres (controlled release form) for the effective management of inflammation. Methods: The solid dispersion (SD) was prepared by melting method using PEG 4000 and tween 80 and formation was confirmed by Differential Scanning Calorimetry (DSC) and Powder X-ray Diffraction (PXRD) studies. Polymeric microspheres loaded with Lornoxicam were prepared by ‘Emulsion Solvent-Evaporation’ method using Eudragit S-100 and Eudragit L-100. Microspheres (MS) were evaluated for drug entrapment efficiency, drug loading, drug content, particle size and in vitro release behaviour. Optimized microspheres (polymer concentration 0.5% w/v and drug concentration 0.1% w/v and solid dispersion (drug: PEG 4000: 4:6) were compressed in the ratio of 1:3 to produce biphasic tablet. The prepared tablets were evaluated for various pre-compression and post-compression parameters. Antiinflammatory activity of the F4, M6 and the combination of SD and Microspheres in a ratio of 1:3 was carried out by Carrageenan induced paw edema method in Wistar rats. Results: The solid dispersions prepared by melting technique showed an enhanced dissolution rate as compared to the pure drug. LXM microspheres exhibited a sustained drug release. In vitro release of lornoxicam from biphasic tablets showed that 20 % of the drug released at the end of first one hour, followed by 33% release at the end of 4th h and maximum release of 94.1 % at the end of 10 h. The prolonged effect continued till the end of 12 h. Results showed that the mixture of MS + SD exhibited 48 % inhibition in 30 min which is increased to 88.63% at the end of 4 h which can be explained by initial burst release from the soluble layer of SD (which gave initial required effective concentration of Lornoxicam) followed by sustained release from matrix of microspheres (which maintained required level of Lornoxicam in blood). Conclusion: A successful modification of the release pattern of LXM was achieved by designing a biphasic tablet comprising of solid dispersion for the effective management of inflammation.