Levantamento da Utilização do Pequi (Caryocar brasiliense camb.) como Agente Antioxidante na Prevenção de Doenças Neurodegenerativas

UNICIÊNCIAS ◽  
2017 ◽  
Vol 21 (2) ◽  
pp. 110
Author(s):  
Erick De Oliveira Lemes ◽  
Michele Maria Carlos Fernandes ◽  
Valeria Paiva Rosa ◽  
Adriano Honorato Nascimento
Keyword(s):  
Free Radicals ◽  
Neurodegenerative Diseases ◽  
Public Health Problem ◽  
Human Organism ◽  
Loss Of Function ◽  
Neuronal Structure ◽  
Fruit Species ◽  
Antioxidant Agent ◽  
Caryocar Brasiliense ◽  
Best Fit

O cerrado é um patrimônio de recursos naturais renováveis, com espécies frutíferas, com características peculiares e intensas. O Caryocar brasiliense Camb. possui atividade antioxidante, conforme estudos realizados, o consumo de pequi regularmente pode agir de forma a minimizar esse desequilíbrio, com a diminuição do nível de radicais livres no organismo humano. As doenças neurodegenerativas levam à perda de função e estrutura neuronal, sendo um grave problema de saúde pública, o número de casos cresce a cada ano. Estas doenças são associadas ao desequilíbrio entre a produção de radicais livres e antioxidantes. O presente estudo teve a finalidade de discutir sobre a importância da utilização do Caryocar brasiliense camb. como agente antioxidante, que pode ser utilizado na prevenção da doença de Alzheimer e doença de Parkinson, caracterizadas como doenças neurodegenerativas. Esta investigação foi caracterizada como pesquisa bibliográfica, a coleta foi realizada nas bases eletrônicas, para avaliação inicial foi realizada leitura dos resumos, com finalidade de selecionar aqueles que melhor se adequaram ao objetivo da pesquisa. A utilização do Caryocar brasiliense Camb. na alimentação é benéfico para a população, de uma forma geral, por apresentar ação antioxidante, o que diminui os danos oxidativos, podendo retardar o envelhecimento precoce das células e evitar o desenvolvimento das doenças neurodegenerativas.Palavras-chave: População. Antioxidante. Doenças neurodenerativas.AbstractThe cerrado is a heritage of renewable natural resources, with fruit species, with peculiar and intense characteristics. The Caryocar brasiliense Camb., has antioxidant activity, according to studies carried out, the consumption of pequi regularly can act in a way to minimize this imbalance, with the reduction of the level of free radicals in the human organism. Neurodegenerative diseases, leads to loss of function and neuronal structure, is a serious public health problem and the number of cases grows each year. These are associated with the imbalance between the production of free radicals and antioxidants. The present study had the purpose of discussing the importance of the use of Caryocar brasiliense camb., as an antioxidant agent that can be used in the prevention of Alzheimer’s disease and Parkinson’s disease, characterized as neurodegenerative diseases. This research was characterized as a bibliographical research, the collection was performed in the electronic databases, for the initial evaluation, the abstracts were read, with the purpose of selecting those that best fit the research objective. The use of Caryocar brasiliense Camb in dietes is beneficial to the population in general, because it has antioxidant action, which decreases oxidative damage, can delay the early cells aging and prevent the neurodegenerative diseases development.Keywords: Population. Antioxidant. Neurodegenerative diseases.

scholarly journals Green Tea Epigallocatechin-3-gallate (EGCG) Targeting Protein Misfolding in Drug Discovery for Neurodegenerative Diseases

Biomolecules ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 767
Author(s):  
Priscila Baltazar Gonçalves ◽  
Ana Carolina Rennó Sodero ◽  
Yraima Cordeiro
Keyword(s):  
Drug Discovery ◽  
Neurodegenerative Diseases ◽  
Green Tea ◽  
Protein Misfolding ◽  
Financial Burden ◽  
Scientific Evidence ◽  
Symptomatic Relief ◽  
Public Health Problem ◽  
Bioactive Compound ◽  
Common Cause

The potential to treat neurodegenerative diseases (NDs) of the major bioactive compound of green tea, epigallocatechin-3-gallate (EGCG), is well documented. Numerous findings now suggest that EGCG targets protein misfolding and aggregation, a common cause and pathological mechanism in many NDs. Several studies have shown that EGCG interacts with misfolded proteins such as amyloid beta-peptide (Aβ), linked to Alzheimer’s disease (AD), and α-synuclein, linked to Parkinson’s disease (PD). To date, NDs constitute a serious public health problem, causing a financial burden for health care systems worldwide. Although current treatments provide symptomatic relief, they do not stop or even slow the progression of these devastating disorders. Therefore, there is an urgent need to develop effective drugs for these incurable ailments. It is expected that targeting protein misfolding can serve as a therapeutic strategy for many NDs since protein misfolding is a common cause of neurodegeneration. In this context, EGCG may offer great potential opportunities in drug discovery for NDs. Therefore, this review critically discusses the role of EGCG in NDs drug discovery and provides updated information on the scientific evidence that EGCG can potentially be used to treat many of these fatal brain disorders.

scholarly journals Early-Onset Parkinson Disease Screening in Patients From Nigeria

2021 ◽  
Vol 11 ◽  
Author(s):  
Lukasz M. Milanowski ◽  
Olajumoke Oshinaike ◽  
Benjamin J. Broadway ◽  
Jennifer A. Lindemann ◽  
Alexandra I. Soto-Beasley ◽  
...  
Keyword(s):  
Functional Analysis ◽  
Parkinson Disease ◽  
Neurodegenerative Diseases ◽  
Early Onset ◽  
Local Population ◽  
Age At Onset ◽  
Compound Heterozygous ◽  
Loss Of Function ◽  
African Countries ◽  
Age Related

Introduction: Nigeria is one of the most populated countries in the world; however, there is a scarcity of studies in patients with age-related neurodegenerative diseases, such as Parkinson disease (PD). The aim of this study was to screen patients with PD including a small cohort of early-onset PD (EOPD) cases from Nigeria for PRKN, PINK1, DJ1, SNCA multiplication, and LRRK2 p.G2019S.Methods: We assembled a cohort of 109 Nigerian patients with PD from the four main Nigerian tribes: Yoruba, Igbo, Edo, and Hausa. Fifteen cases [14 from the Yoruba tribe (93.3%)] had EOPD (defined as age-at-onset <50 years). All patients with EOPD were sequenced for the coding regions of PRKN, PINK1, and DJ1. Exon dosage analysis was performed with a multiplex ligation-dependent probe amplification assay, which also included a SNCA probe and LRRK2 p.G2019S. We screened for LRRK2 p.G2019S in the entire PD cohort using a genotyping assay. The PINK1 p.R501Q functional analysis was conducted.Results: In 15 patients with EOPD, 22 variants were observed [PRKN, 9 (40.9%); PINK1, 10 (45.5%); and DJ1, 3 (13.6%)]. Three (13.6%) rare, nonsynonymous variants were identified, but no homozygous or compound heterozygous carriers were found. No exonic rearrangements were present in the three genes, and no carriers of SNCA genomic multiplications or LRRK2 p.G2019S were identified. The PINK1 p.R501Q functional analysis revealed pathogenic loss of function.Conclusion: More studies on age-related neurodegenerative diseases are needed in sub-Saharan African countries, including Nigeria. Population-specific variation may provide insight into the genes involved in PD in the local population but may also contribute to larger studiesperformed in White and Asian populations.

scholarly journals P2-126: LOSS-OF-FUNCTION CODING AND NON-CODING VARIANTS IN TET2 ARE ASSOCIATED WITH NEURODEGENERATIVE DISEASES

2019 ◽  
Vol 15 ◽  
pp. P620-P620
Author(s):  
J. Nicholas Cochran ◽  
Ethan G. Geier ◽  
Juliana Acosta-Uribe ◽  
Michelle L. Thompson ◽  
Michelle D. Amaral ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Loss Of Function ◽  
Coding Variants

scholarly journals PrP is a central player in toxicity mediated by soluble aggregates of neurodegeneration-causing proteins

2019 ◽  
Vol 139 (3) ◽  
pp. 503-526 ◽  
Author(s):  
Grant T. Corbett ◽  
Zemin Wang ◽  
Wei Hong ◽  
Marti Colom-Cadena ◽  
Jamie Rose ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Cortical Neurons ◽  
Lewy Bodies ◽  
Public Health Problem ◽  
Therapeutic Targeting ◽  
Neuronal Proteins ◽  
Neuritic Dystrophy ◽  
Soluble Aggregates ◽  
Blocking Antibodies

AbstractNeurodegenerative diseases are an enormous public health problem, affecting tens of millions of people worldwide. Nearly all of these diseases are characterized by oligomerization and fibrillization of neuronal proteins, and there is great interest in therapeutic targeting of these aggregates. Here, we show that soluble aggregates of α-synuclein and tau bind to plate-immobilized PrP in vitro and on mouse cortical neurons, and that this binding requires at least one of the same N-terminal sites at which soluble Aβ aggregates bind. Moreover, soluble aggregates of tau, α-synuclein and Aβ cause both functional (impairment of LTP) and structural (neuritic dystrophy) compromise and these deficits are absent when PrP is ablated, knocked-down, or when neurons are pre-treated with anti-PrP blocking antibodies. Using an all-human experimental paradigm involving: (1) isogenic iPSC-derived neurons expressing or lacking PRNP, and (2) aqueous extracts from brains of individuals who died with Alzheimer’s disease, dementia with Lewy bodies, and Pick’s disease, we demonstrate that Aβ, α-synuclein and tau are toxic to neurons in a manner that requires PrPC. These results indicate that PrP is likely to play an important role in a variety of late-life neurodegenerative diseases and that therapeutic targeting of PrP, rather than individual disease proteins, may have more benefit for conditions which involve the aggregation of more than one protein.

Synthetic Lapachol Derivatives Relax Guinea-Pig Ileum by Blockade of the Voltage-Gated Calcium Channels

2010 ◽  
Vol 65 (9-10) ◽  
pp. 627-636
Author(s):  
Fabiana de A. Cavalcante ◽  
Fabio De S. Monteiro ◽  
Italo Rossi R. Martins ◽  
Ticiano P. Barbosa ◽  
Celso de A Camara ◽  
...  
Keyword(s):  
Free Radicals ◽  
Guinea Pig ◽  
Calcium Channels ◽  
Action Mechanism ◽  
Guinea Pig Ileum ◽  
Spasmolytic Activity ◽  
Tonic Component ◽  
Voltage Gated ◽  
Voltage Gated Calcium Channels ◽  
Antioxidant Agent

The present study was designed to further evaluate a possible spasmolytic activity of synthetic lapachol derivatives, norlapachol, α-norlapachone, β-norlapachone and hydro-hydroxy- norlapachol (HH-norlapachol), on guinea-pig ileum. In guinea-pig ileum, except for norlapachol, all naphthoquinones inhibited the phasic contractions induced by carbachol or histamine. Even when the ileum was pre-contracted with KCl, carbachol or histamine, all naphthoquinones induced relaxation, suggesting that these naphthoquinones could be acting on the voltage-gated calcium channels (CaV). As the tonic component this contraction is maintained mainly by the opening of the CaV, we hypothesized that these naphthoquinones might be acting on these channels. This hypothesis was confirmed by the observation that norlapachol (pD’2 = 4.99), α-norlapachone (pD’2 = 4.49), β-norlapachone (pD’2 = 6.33), and HH-norlapachol (pD’2 = 4.53) antagonized the contractions induced by CaCl2 in depolarizing medium nominally without Ca2+. As β-norlapachone was the most potent we decided to continue the study of its action mechanism. The fact that this naphthoquinone has inhibited the tonic contractions induced by S-(-)-Bay K8644 [EC50 = (1.6 ± 0.30) · 10-5 M] suggests that the Ca2+ channel involved belongs to the type L (CaV1.2). In addition, in the functional level, the spasmolytic effect of β-norlapachone does not involve participation of free radicals, since its curve of relaxation was unchanged in the presence of glutathione, an antioxidant agent.

scholarly journals Research on an antioxidant capacity of honeys

2012 ◽  
Vol 59 (1) ◽  
pp. 265-269 ◽  
Author(s):  
Elżbieta Hołderna-Kędzia ◽  
Bogdan Kędzia
Keyword(s):  
Ascorbic Acid ◽  
Natural Products ◽  
Free Radicals ◽  
Antioxidant Capacity ◽  
Antioxidative Activity ◽  
Polyphenolic Compounds ◽  
Human Organism ◽  
Oxidation Activity ◽  
Harmful Action ◽  
Antioxidative Agents

Human organism is exposed to harmful action of free radicals which are produced as well endogenically as egzogenically. The oxidation activity of free radicals can lead to the conversion of systemic biomolecules. As a consequence, there is a threat of, many severe diseases. Antioxidative agents which occur in natural products (also in honey) raise a possibility of protection against the harmful action of above mentioned radicals. Polyphenolic compounds - flavonoids, phenolic acids and ascorbic acid - are the most important antioxidative agents. The research of many authors proves that honey, given orally, shows an antioxidative activity. The level of antioxidative agents in serum after the consumption of honey is high and surpasses the antioxidative activity of tea. Dark honeys (honeydew and heather) have considerably higher antioxidative activity in comparison to light ones (acacia, lime, polyfloral).

scholarly journals Contribution of rare variant associations to neurodegenerative disease presentation

2021 ◽  
Vol 6 (1) ◽  
Author(s):  
Allison A. Dilliott ◽  
Abdalla Abdelhady ◽  
Kelly M. Sunderland ◽  
Sali M. K. Farhan ◽  
Agessandro Abrahao ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Neurodegenerative Disease ◽  
Rare Variant ◽  
Genetic Factors ◽  
Association Studies ◽  
Loss Of Function ◽  
Phenotypic Effect ◽  
Association Analyses ◽  
Individual Gene ◽  
Genetic Overlap

AbstractGenetic factors contribute to neurodegenerative diseases, with high heritability estimates across diagnoses; however, a large portion of the genetic influence remains poorly understood. Many previous studies have attempted to fill the gaps by performing linkage analyses and association studies in individual disease cohorts, but have failed to consider the clinical and pathological overlap observed across neurodegenerative diseases and the potential for genetic overlap between the phenotypes. Here, we leveraged rare variant association analyses (RVAAs) to elucidate the genetic overlap among multiple neurodegenerative diagnoses, including Alzheimer’s disease, amyotrophic lateral sclerosis, frontotemporal dementia (FTD), mild cognitive impairment, and Parkinson’s disease (PD), as well as cerebrovascular disease, using the data generated with a custom-designed neurodegenerative disease gene panel in the Ontario Neurodegenerative Disease Research Initiative (ONDRI). As expected, only ~3% of ONDRI participants harboured a monogenic variant likely driving their disease presentation. Yet, when genes were binned based on previous disease associations, we observed an enrichment of putative loss of function variants in PD genes across all ONDRI cohorts. Further, individual gene-based RVAA identified significant enrichment of rare, nonsynonymous variants in PARK2 in the FTD cohort, and in NOTCH3 in the PD cohort. The results indicate that there may be greater heterogeneity in the genetic factors contributing to neurodegeneration than previously appreciated. Although the mechanisms by which these genes contribute to disease presentation must be further explored, we hypothesize they may be a result of rare variants of moderate phenotypic effect contributing to overlapping pathology and clinical features observed across neurodegenerative diagnoses.

scholarly journals Oxidative stress

2012 ◽  
Vol 66 (3-4) ◽  
pp. 273-283
Author(s):  
Jelka Stevanovic ◽  
Suncica Borozan ◽  
Tatjana Bozic ◽  
Slavoljub Jovic ◽  
Tatjana Djekic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Hypochlorous Acid ◽  
Ion Homeostasis ◽  
Peroxyl Radicals ◽  
Biological Macromolecules ◽  
Loss Of Function ◽  
Cellular Membranes ◽  
Rna Molecules ◽  
Dna And Rna

The unceasing need for oxygen is in contradiction to the fact that it is in fact toxic to mammals. Namely, its monovalent reduction can have as a consequence the production of short-living, chemically very active free radicals and certain non-radical agents (nitrogen-oxide, superoxide-anion-radicals, hydroxyl radicals, peroxyl radicals, singlet oxygen, peroxynitrite, hydrogen peroxide, hypochlorous acid, and others). There is no doubt that they have numerous positive roles, but when their production is stepped up to such an extent that the organism cannot eliminate them with its antioxidants (superoxide-dismutase, glutathione-peroxidase, catalase, transferrin, ceruloplasmin, reduced glutathion, and others), a series of disorders is developed that are jointly called ?oxidative stress.? The reactive oxygen species which characterize oxidative stress are capable of attacking all main classes of biological macromolecules, actually proteins, DNA and RNA molecules, and in particular lipids. The free radicals influence lipid peroxidation in cellular membranes, oxidative damage to DNA and RNA molecules, the development of genetic mutations, fragmentation, and the altered function of various protein molecules. All of this results in the following consequences: disrupted permeability of cellular membranes, disrupted cellular signalization and ion homeostasis, reduced or loss of function of damaged proteins, and similar. That is why the free radicals that are released during oxidative stress are considered pathogenic agents of numerous diseases and ageing. The type of damage that will occur, and when it will take place, depends on the nature of the free radicals, their site of action and their source.

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