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1.
Int J Dev Neurosci ; 84(3): 163-176, 2024 May.
Article in English | MEDLINE | ID: mdl-38488315

ABSTRACT

INTRODUCTION: Recent research indicates that some brain structures show alterations in conditions such as Autism Spectrum Disorder (ASD). Among them, are the basal ganglia that are involved in motor, cognitive and behavioral neural circuits. OBJECTIVE: Review the literature that describes possible volumetric alterations in the basal ganglia of individuals with ASD and the impacts that these changes have on the severity of the condition. METHODOLOGY: This systematic review was registered in the design and reported according to the PRISMA Items and registered in PROSPERO (CRD42023394787). The study analyzed data from published clinical, case-contemplate, and cohort trials. The following databases were consulted: PubMed, Embase, Scopus, and Cochrane Central Register of Controlled Trials, using the Medical Subject Titles (MeSH) "Autism Spectrum Disorder" and "Basal Ganglia". The last search was carried out on February 28, 2023. RESULTS: Thirty-five eligible articles were collected, analyzed, and grouped according to the levels of alterations. CONCLUSION: The present study showed important volumetric alterations in the basal ganglia in ASD. However, the examined studies have methodological weaknesses that do not allow generalization and correlation with ASD manifestations.


Subject(s)
Autism Spectrum Disorder , Basal Ganglia , Humans , Autism Spectrum Disorder/diagnostic imaging , Autism Spectrum Disorder/pathology , Autism Spectrum Disorder/physiopathology , Basal Ganglia/pathology , Basal Ganglia/diagnostic imaging
2.
Int J Mol Sci ; 24(13)2023 Jul 07.
Article in English | MEDLINE | ID: mdl-37446369

ABSTRACT

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.


Subject(s)
Alzheimer Disease , Neurodegenerative Diseases , Humans , Vitamin E/pharmacology , Vitamin E/therapeutic use , Neurodegenerative Diseases/drug therapy , Alzheimer Disease/drug therapy , Cognition/physiology , Models, Theoretical
3.
Acta Neurobiol Exp (Wars) ; 82(4): 448-461, 2022.
Article in English | MEDLINE | ID: mdl-36748968

ABSTRACT

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.


Subject(s)
Hippocampus , Linseed Oil , Neuroglia , Physical Conditioning, Animal , Animals , Male , Rats , Astrocytes/metabolism , Dietary Supplements , Glial Fibrillary Acidic Protein/metabolism , Hippocampus/metabolism , Linseed Oil/pharmacology , Neuroglia/metabolism , Rats, Wistar
4.
Acta Neurobiol Exp (Wars) ; 81(1): 58-68, 2021.
Article in English | MEDLINE | ID: mdl-33949162

ABSTRACT

Forced swimming is a common exercise method used for its low cost and easy management, as seen in studies with the hippocampus. Since it is applied for varied research purposes many protocols are available with diverse aspects of physical intensity, time and periodicity, which produces variable outcomes. In the present study, we performed a systematic review to stress the neurobiological effects of forced swim exercise on the rodent hippocampus. Behavior, antioxidant levels, neurotrophins and inflammatory markers were the main topics examined upon the swimming effects. Better results among these analyses were associated with forced exercise at moderate intensity with an adaptation period and the opposite for continuous exhausting exercises with no adaptation. On further consideration, a standard swimming protocol is necessary to reduce variability of results for each scenario investigated about the impact of the forced swimming on the hippocampus.Forced swimming is a common exercise method used for its low cost and easy management, as seen in studies with the hippocampus. Since it is applied for varied research purposes many protocols are available with diverse aspects of physical intensity, time and periodicity, which produces variable outcomes. In the present study, we performed a systematic review to stress the neurobiological effects of forced swim exercise on the rodent hippocampus. Behavior, antioxidant levels, neurotrophins and inflammatory markers were the main topics examined upon the swimming effects. Better results among these analyses were associated with forced exercise at moderate intensity with an adaptation period and the opposite for continuous exhausting exercises with no adaptation. On further consideration, a standard swimming protocol is necessary to reduce variability of results for each scenario investigated about the impact of the forced swimming on the hippocampus.


Subject(s)
Antioxidants/metabolism , Hippocampus/physiology , Physical Conditioning, Animal/physiology , Swimming/physiology , Animals , Rodentia , Time Factors
5.
Curr Neuropharmacol ; 17(5): 406-421, 2019.
Article in English | MEDLINE | ID: mdl-29338678

ABSTRACT

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.


Subject(s)
Alzheimer Disease/drug therapy , Curcumin/administration & dosage , Neuroprotective Agents/administration & dosage , Plant Extracts/administration & dosage , Alzheimer Disease/metabolism , Alzheimer Disease/pathology , Alzheimer Disease/prevention & control , Amyloid beta-Peptides/metabolism , Animals , Curcuma/chemistry , Curcumin/pharmacology , Dietary Supplements , Humans , Neurofibrillary Tangles/metabolism , Neuroprotective Agents/pharmacology , Plant Extracts/pharmacology , Randomized Controlled Trials as Topic
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