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Parkinson's disease (PD) is designated as a convoluted nerve cell devastating disorder that encompasses the profound declination of dopaminergic (DArgic) nerve cells of the mesencephalon region. The condition is sketched by four eminent motor manifestations, namely, slow movement, muscle tension, shaking, and disrupted balance, but the pathology behind these manifestations is still vague. Modern-day medicinal treatment emphasizes curbing the manifestations via introducing a gold standard (levodopa) instead of forestalling the DArgic nerve cell destruction. Therefore, the invention and utilization of novel neuroprotective candidates are of paramount importance in overcoming PD. Vitamins are organic molecules engaged in the modulation of evolution, procreation, biotransformation, and other operations of the body. Numerous studies employing varying experimental models have promulgated a prominent linkage between vitamins and PD. Vitamins, owing to their antioxidant and gene expression modulation abilities, might be efficacious in PD therapy. Recent corroborations depict that adequate augmentation of vitamins might de-escalate the manifestations and emergence of PD; however, the safety of daily vitamin intake must be considered. By assembling the comprehensive information obtained from existing publications via searching various renowned medical portals, the investigators render in-depth insights into the physiological association amongst vitamins (D, E, B3, and C) and PD and concerned pathological processes and their safeguarding actions in varied PD models. Furthermore, the manuscript delineates the remedial aptitude of vitamins in PD therapy. Conclusively, augmentation of vitamins (owing to their antioxidant and gene expression regulation capabilities) might appear as a novel and terribly efficacious ancillary therapeutic approach for PD., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Alzheimer's disease or senile dementia is principally acknowledged by the gradual accumulation of neurotoxic amyloid- β protein in the brain and is considered as the initial event of the phenomenon of this asymptomatic ailment. It prompts the decline in cognitive performance, standard psychiatric functioning, and neuronal transmission across the brain. Significant inferences were withdrawn by utilizing the recently introduced disease-modifying anti- amyloid- β immunotherapy developed after performing the clinical and preclinical controlled trials to cure the neurodegenerative malady. This strategy is worthwhile because of the clinical relevance and specific targeted approach that exhibited the quenched immunotherapeutic effects and encouraged clinical findings. In vitro fabricated, anti- amyloid- β recombinant monoclonal antibodies are passively employed to promote clearance and antagonize the aggregation and synthesis of neurotoxic and degenerative aggregates of amyloid-β. Thus, passive immunotherapy has an adequate impact on treating this disorder, and currently, some other monoclonal pharmacological molecules are under clinical trials to defeat this severe exacerbation with more efficacy and clinical benefits. This review compendiously discusses the anti-amyloid-β immunotherapy, which will provide a more proficient framework to be employed as a potential therapeutic approach., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

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