A5089942384- Sleep and Wakefulness Research
- Nuclear Structure and Function
- Dietary Effects on Health
- Circadian rhythm and melatonin
- Regulation of Appetite and Obesity
- Mitochondrial Function and Pathology
- Autophagy in Disease and Therapy
- RNA Research and Splicing
- Breastfeeding Practices and Influences
- Oral Health Pathology and Treatment
- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Genetic Neurodegenerative Diseases
- Turtle Biology and Conservation
- Cholinesterase and Neurodegenerative Diseases
- Advanced Memory and Neural Computing
- Neurological and metabolic disorders
- Computational Drug Discovery Methods
- Autism Spectrum Disorder Research
- Pancreatic function and diabetes
- PARP inhibition in cancer therapy
- Ichthyology and Marine Biology
- Fish biology, ecology, and behavior
- Biochemical Analysis and Sensing Techniques
- Parkinson's Disease Mechanisms and Treatments
University of Coimbra
2015-2025
Universidade Federal do Rio de Janeiro
2001-2018
Universidade Federal de Minas Gerais
2003
Significance Autophagy impairment is a major hallmark of aging, and any intervention that enhances autophagy potential interest to delay aging. However, it was described the hypothalamus brain area with key role on whole-body In present study, we show an endogenous molecule produced by hypothalamus, neuropeptide Y (NPY), stimulates in rodent hypothalamus. Because both hypothalamic NPY levels decrease age, better understanding neuronal regulation may provide new putative therapeutic...
Caloric restriction is an anti-aging intervention known to extend lifespan in several experimental models, at least part, by stimulating autophagy. increases neuropeptide Y (NPY) the hypothalamus and plasma ghrelin, a peripheral gut hormone that acts modulate energy homeostasis. NPY ghrelin have been shown be neuroprotective different brain areas induce physiological modifications similar those induced caloric restriction. However, effect of autophagy cortical neurons currently not known....
The estimated mean intestinal coefficients of Leporinus friderici Bloch, 1794 and L. taeniofasciatus Britski, 1997, from the Upper Tocantins River, central‐western Brazil, were 1·25±0·15 1·14±0·07, respectively. external surfaces lips have taste buds. histological structure is composed four layers: mucosa, submucosa, muscular, serosa. No muscularis mucosa detected. oesophageal epithelium stratified in pseudostratified , latter with PAS+ basal cells eosinophilic apical cells. A thick layer...
Caloric restriction has been shown to robustly ameliorate age-related diseases and prolong lifespan in several model organisms, these beneficial effects are dependent on the stimulation of autophagy.Autophagy dysfunction contributes accumulation altered macromolecules, is a key mechanism promoting aging disorders, as neurodegenerative ones.We have previously that caloric (CR), CR mimetics Neuropeptide Y (NPY) ghrelin, stimulate autophagy rat cortical neurons, however by unknown molecular...
Autism Spectrum Disorders (ASDs) are a group of neurodevelopmental pathologies whose current treatment is neither curative nor effective. Anthocyanins naturally occurring compounds abundant in blueberries and other red fruits which have been shown to be successful the several neurological diseases, at least vitro vivo disease models. The aim present work was study ability an anthocyanin-rich extract (ARE) obtained from Portuguese alleviate autism-like symptoms valproic acid (VPA) mouse model...
Abstract Machado-Joseph disease (MJD) is caused by an abnormal CAG repeat expansion in the ATXN3 gene, leading to expression of a mutant ataxin-3 (mutATXN3) protein. MJD patients exhibit wide range clinical symptoms, including motor incoordination. Emerging evidence highlights circadian rhythm disruptions as early indicators and potential risk factors for progression neurodegenerative conditions. Circadian rhythms are regulated internal clocks, with suprachiasmatic nucleus (SCN) acting...
Abstract The hypothalamus has been recognized as a regulator of whole-body aging. Neuropeptide Y (NPY), highly abundant in the central nervous system and produced by hypothalamus, enhances autophagy this brain region mediates triggered caloric restriction, suggesting potential role restriction mimetic an aging regulator. Considering that hypothalamic NPY levels decline during aging, we investigated if reestablishment mitigate phenotype, using mouse model premature – Zmpste24 −/− mouse....
Abstract Hutchinson‐Gilford progeria syndrome (HGPS) is a rare and fatal genetic condition that arises from single nucleotide alteration in the LMNA gene, leading to production of defective lamin A protein known as progerin. The accumulation progerin accelerates onset dramatic premature aging phenotype children with HGPS, characterized by low body weight, lipodystrophy, metabolic dysfunction, skin, musculoskeletal age‐related dysfunctions. In most cases, these die cardiovascular dysfunction...
Oral manifestations may be the first signs of hematologic diseases, and occur due to disease itself or treatment.
Abstract Hutchinson-Gilford progeria syndrome (HGPS, or classical progeria) is a rare genetic disorder, characterized by premature aging, and caused de novo point mutation (C608G) within the lamin A/C gene (LMNA), producing an abnormal A protein, termed progerin. Accumulation of progerin causes nuclear abnormalities cell cycle arrest ultimately leading to cellular senescence. Autophagy impairment hallmark rescue this proteostasis mechanism delays aging progression in HGPS cells. We have...
ATXN2 gene, encoding for ataxin-2, is located in a trait locus obesity. Atxn2 knockout (KO) mice are obese and insulin resistant; however, the cause this phenotype still unknown. Moreover, several findings suggest ataxin-2 as metabolic regulator, but role of protein hypothalamus was never studied before. The aim work to understand if modulation could play regulation. Ataxin-2 overexpressed/re-established C57Bl6/Atxn2 KO fed either chow or high-fat diet (HFD). This delivery achieved through...
A disease-modifying therapy for Alzheimer's disease (AD) is still an unmet clinical need. The formation of amyloid-β (Aβ) requires the initial cleavage protein precursor (AβPP) by BACE1 (beta-site AβPP cleaving enzyme 1), which a prime therapeutic target AD.We aimed to design and develop selective inhibitor suitable AD treatment.The new inhibitors consist on chimeric peptide including sequence related human Swedish mutant form (AβPPswe) conjugated with TAT carrier that facilitates cell...
Objetivo: o presente estudo foi realizado com objetivo de comparar a eficácia uma fórmula infantil pré-espessada (Nan AR) convencional, espessamento caseiro, amido milho, na redução episódios regurgitações e vômitos lactentes refluxo gastroesofágico (RGE). Métodos: foram estudadas 100 crianças, menores 12 meses idade, que não faziam uso leite materno exclusivo. Por sorteio, 48 receberam 52 AR), comparação dos resultados clínicos após 3 meses. Resultados: houve diferença estatisticamente...
Abstract Hutchinson-Gilford progeria syndrome (HGPS) is a rare and fatal genetic condition arising from single nucleotide alteration in the LMNA gene, which leads to production of defective lamin A protein known as progerin. The buildup progerin hastens onset premature expedited aging. Patients with HGPS exhibit short stature, low body weight, lipodystrophy, metabolic dysfunction, skin musculoskeletal abnormalities and, most cases, die cardiovascular disease by their early teenage years....
Hutchinson-Gilford progeria syndrome (HGPS), a lethal rare genetic disorder, is characterized by premature aging. HGPS most commonly caused de novo point mutation (C608G) within the lamin A/C gene (LMNA), producing an abnormal A protein termed progerin. We have showed that Neuropeptide Y (NPY) increases autophagy in hypothalamus (1), brain area recently identified as central regulator of whole-body aging (2). In addition, we also observed NPY mediates caloric restriction-induced (1). Some...