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Cognitive impairment and dementia are the most frequently occurring nonmotor symptoms in Parkinson’s disease (PD), yet these symptoms are mostly overlooked and are not diagnosed and treated exceptionally like the cardinal motor symptoms in clinical practice. It is only in the late twentieth century that dementia has been recognized as a major clinical manifestation in PD. The possible mechanisms that cause dementia are complex with different patterns of cognitive behavior that disrupt the patient’s quality of life. It is preeminently considered that the cholinergic denervation in the basal forebrain region mediates dementia in PD. So far, dopamine-based therapy is the key objective in the treatment of PD and the nonmotor symptoms are mostly neglected. Interestingly, the loss of Tyrosine kinase receptor-A (TrkA) signaling in basal forebrain results in neuronal atrophy, which precedes cholinergic denervation and cognitive impairment. Nerve Growth Factor (NGF) binds to TrkA receptors, inducing a cascade of events like PI-3Kinase/Akt and MAPK signaling pathways that render cholinergic degeneration and upregulate the choline acetyltransferase activity and neuronal differentiation. Hence, TrkA receptor activation by small molecules might attenuate the dementia symptoms associated with PD, and may be targeted as a novel treatment strategy along with regular clinical agents.

Advancements in brain imaging techniques have emerged as a significant tool in detecting Alzheimer's disease (AD) progression. The complicated cascade of AD progression can be detected using radio imaging, especially with Positron emission tomography (PET). The review focus on recently introduced investigational PET tracers targeting neurofibrillary tau aggregates found typically in AD. Herein, we also address the use of different PET tracers and the clinical implementation of established and newer generation tracers. This review also intends to discuss the importance of several PET radiotracers and challenges in PET imaging.

Purpose The purpose of this work is to investigate the optimization of automotive wheel rim using ansys. Design Methodology Approach In this study heavy stresses in the rim was developed, the critical stress and number cycles to failure were to be found. The purpose of the car wheel rim was to provide a firm base to hold the tire .Its dimensions and shape should be suitable to accommodate the particular tire required for the vehicle .In this study ,a car wheel rim considered .The wheel rim was designed by using modeling software SOLID WORKS V13.The solid model was then imported to ANSYS for static analysis. Findings The experimental results indicate that the static analysis is carried out by considering the three different materials namely steel alloy, alluminium alloy and their relative performance have been observed .In addition to this the rim is subjected to fatigue analysis using MSV fatigue software and its performance is observed .The results of static and fatigue analysis obtained from three different materials reveals that the steel alloy is the best material of wheel rim. Originality value This paper explains the effect of different materials on the wheel through by vonmises stresses and number of cycles in fatigue analysis. R. Ashok Kumar | G. Amarnath | K. Padmanaban | S. Karuppusamy | I. Justin Antony Raj "Experimental Studies of Optimization of Automotive wheel Rim using ANSYS" Published in International Journal of Trend in Scientific Research and Development (ijtsrd), ISSN: 2456-6470, Volume-3 | Issue-3 , April 2019, URL: https://www.ijtsrd.com/papers/ijtsrd22778.pdf

Diosgenin is a neurosteroid derived from the plants and has been previously reported for its numerous health beneficial properties, such as anti-arrhythmic, hypolipidemic, and antiproliferative effects. Although several studies conducted earlier suggested cognition enhancement actions of diosgenin against neurodegenerative disorders, but the molecular mechanisms underlying are not clearly understood. In the present study, we investigated the neuroprotective effect of diosgenin in the wistar rats that received an intracerebroventricular injection of Amyloid-β (1–42) peptides, representing a rodent model of Alzheimer’s disease (AD). Animals were treated with 100 and 200 mg/kg/p.o of diosgenin for 28 days, followed by Amyloid-β (1–42) peptides infusion. Animals were assessed for the spatial learning and memory by using radial arm maze and passive avoidance task. Subsequently, animals were euthanized and brains were collected for biochemical estimations and histopathological studies. Our results revealed that, diosgenin administration dose dependently improved the spatial learning and memory and protected the animals from Amyloid-β (1–42) peptides induced disrupted cognitive functions. Further, biochemical analysis showed that diosgenin successfully attenuated Amyloid-β (1–42) mediated plaque load, oxidative stress, neuroinflammation and elevated acetylcholinesterase activity. In addition, histopathological evaluation also supported neuroprotective effects of diosgenin in hippocampus of rat brain when assessed using hematoxylin-eosin and Cresyl Violet staining. Thus, the aforementioned effects suggested protective action of diosgenin against Aβ (1–42) induced neuronal damage and thereby can serve as a potential therapeutic candidate for AD.

Background: There is a constant hunt for the development of new therapeutic alternative to address Alzheimer's disease (AD) due to its failing attempts in the evolution of new therapies and suboptimal results from the existing pharmacological interventions for the treatment of this severe neurodegenerative disease. Vernonia anthelmintica is an extensively used medicinal plant in Indian traditional medicine with wide range of therapeutic values. However, there is insufficient scientific documentation available for its protective effect against cognitive disorders. Objectives: The objective of the current investigation is to explore the neuroprotective activity of methanolic extract of V. anthelmintica (MEVA) in amyloid-beta (Aβ) (1–42) infused sporadic model of AD. Materials and Methods: Adult healthy male Wistar rats were treated orally with 250 mg/kg and 500 mg/kg of MEVA for 28 days, after a week from intracerebroventricular (i.c.v) infusion of Aβ (1–42) peptides followed by assessment of neurobehavioral deficits. Subsequently, animals were euthanized and brains were collected for estimation and quantification of neurochemical biomarkers including antioxidant enzymes, neurotransmitters, plaque load, and inflammatory mediators. Results: Dose-dependent reversal of cognitive impairment was observed upon MEVA treatment in amyloid intoxicated rats as corroborated by improved learning and memory and diminished oxidative stress, cholinergic hypofunction, and neuroinflammation induced by Aβ (1–42). Conclusion: Collectively, evidence-based data suggested the promising neurotherapeutic potential of V. anthelmintica and thereby can stand as a novel entity for curbing AD pathology.

Neurological disorders such as Alzheimer’s Disease (AD), Parkinsons’s Disease (PD) and Cerebral Ischemic Stroke (CIS) are responsible for morbidities in almost a billion people and it is rising with increase in older population. AD is responsible for most dementia cases reported worldwide and is marked by the loss of memory and aggregation of Amyloid beta peptide (AsP) and Neurofibrillary tangle (NFT). Oxidative stress, apoptosis are few of the factors that influence the pathophysiology. PD is characterized by genetic abnormalities, mitochondrial dysfunction, oxidative stress, excitotoxicity, calcium and iron overload and neuroinflammation and manifests as rigidity and bradykinesia. CIS is caused by reduced cerebral blood flow and impaired metabolic processes. The generation of free radicals and elevation of Ca2+ levels along with inflammatory cytokines, carries out the process. The use of plants for various disease condition is as old as history. The recent advancements in scientific drug development has hastened the discovery process and has opened doors to new discoveries having potential in treatment of neurological disorders such as AD, PD and CIS. These investigations has resulted in discovery of plants and plant extracts with potential neuroprotective effects. However, these discoveries require further validation and scientific proofs to be applied in clinical scenario. Interestingly, these plant based treatments can be co-administered with existing drugs or can be even used as monotherapy, depending on the advancements in this field.