Vitamin E and Its Molecular Effects in Experimental Models of Neurodegenerative Diseases.

With the advancement of in vivo studies and clinical trials, the pathogenesis of neurodegenerative diseases has been better understood. However, gaps still need to be better elucidated, which justifies the publication of reviews that explore the mechanisms related to the development of these diseases. Studies show that vitamin E supplementation can protect neurons from the damage caused by oxidative stress, with a positive impact on the prevention and progression of neurodegenerative diseases. Thus, this review aims to summarize the scientific evidence of the effects of vitamin E supplementation on neuroprotection and on neurodegeneration markers in experimental models. A search for studies published between 2000 and 2023 was carried out in the PubMed, Web of Science, Virtual Health Library (BVS), and Embase databases, in which the effects of vitamin E in experimental models of neurodegeneration were investigated. A total of 5669 potentially eligible studies were identified. After excluding the duplicates, 5373 remained, of which 5253 were excluded after checking the titles, 90 articles after reading the abstracts, and 11 after fully reviewing the manuscripts, leaving 19 publications to be included in this review. Experiments with in vivo models of neurodegenerative diseases demonstrated that vitamin E supplementation significantly improved memory, cognition, learning, motor function, and brain markers associated with neuroregeneration and neuroprotection. Vitamin E supplementation reduced beta-amyloid (Aß) deposition and toxicity in experimental models of Alzheimer's disease. In addition, it decreased tau-protein hyperphosphorylation and increased superoxide dismutase and brain-derived neurotrophic factor (BDNF) levels in rodents, which seems to indicate the potential use of vitamin E in preventing and delaying the progress of degenerative lesions in the central nervous system.

Physical exercise and flaxseed oil supplementation influence the glial plasticity in the rat hippocampus.

Brain benefits from physical exercise associated with antioxidant supplements such as flaxseed oil. This low cost and simple association may improve hippocampal plasticity, which may work as a preventive and effective therapy in neuroprotection and neuroplasticity processes. This work evaluated the effects of physical exercise with flaxseed oil supplementation (Linum usitatissimum L.) in the hippocampus of Wistar rats. We separated male Wistar rats into four experimental groups: control group (sedentary), a sedentary group with a supplemental diet of flaxseed oil, a group under exercise program with flaxseed oil supplementation, and a group exclusively under exercise program. The swimming exercise consisted of a progressive 28­day protocol followed by behavioral assessment, brain perfusion, microtomy, immunohistochemistry for glial fibrillary acidic protein (GFAP), cellular morphology, and optical density analysis. We used the ANOVA test with Tukey's post­test for behavioral analysis. The exercise program with flaxseed oil supplementation was able to alter the GFAP expression in astrocytes in the CA1, CA3 and dentate gyrus regions of the hippocampus and modulate the behavioral aspects of memory and anxiety.

Supplementation with Curcuma longa Reverses Neurotoxic and Behavioral Damage in Models of Alzheimer's Disease: A Systematic Review.

BACKGROUND: The formation of senile plaques and neurofibrillary tangles of the tau protein are the main pathological mechanism of Alzheimer's disease (AD). Current therapies for AD offer discrete benefits to the clinical symptoms and do not prevent the continuing degeneration of neuronal cells. Therefore, novel therapeutic strategies have long been investigated, where curcumin (Curcuma longa) has shown some properties that can prevent the deleterious processes involved in neurodegenerative diseases. OBJECTIVE: The aim of the present work is to review studies that addressed the effects of curcumin in experimental models (in vivo and in vitro) for AD. METHOD: This study is a systematic review conducted between January and June 2017, in which a consultation of scientific articles from indexed periodicals was carried out in Science Direct, United States National Library of Medicine (PubMed), Cochrane Library and Scielo databases, using the following descriptors: "Curcuma longa", "Curcumin" and "Alzheimer's disease". RESULTS: A total of 32 studies were analyzed, which indicated that curcumin supplementation reverses neurotoxic and behavioral damages in both in vivo and in vitro models of AD. CONCLUSION: The administration of curcumin in experimental models seems to be a promising approach in AD, even though it is suggested that additional studies must be conducted using distinct doses and through other routes of administration.