Susana Cardoso

ORCID: 0000-0002-9866-933X
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About
Contact & Profiles
Research Areas
  • Mitochondrial Function and Pathology
  • Alzheimer's disease research and treatments
  • Adipose Tissue and Metabolism
  • Biochemical effects in animals
  • Neurological Disorders and Treatments
  • Pancreatic function and diabetes
  • Autophagy in Disease and Therapy
  • Parkinson's Disease Mechanisms and Treatments
  • Biochemical Acid Research Studies
  • Diet and metabolism studies
  • Metabolism, Diabetes, and Cancer
  • Genetic Neurodegenerative Diseases
  • Tryptophan and brain disorders
  • Neuroscience and Neuropharmacology Research
  • Natural Antidiabetic Agents Studies
  • Metabolism and Genetic Disorders
  • Neurological Disease Mechanisms and Treatments
  • Electron Spin Resonance Studies
  • Cardiac Ischemia and Reperfusion
  • Genetics and Neurodevelopmental Disorders
  • Cholinesterase and Neurodegenerative Diseases
  • Advanced Glycation End Products research
  • Anesthesia and Neurotoxicity Research
  • Cancer, Hypoxia, and Metabolism
  • Endoplasmic Reticulum Stress and Disease

University of Coimbra
2015-2024

Centro de Neurociências e Biologia Celular
2010-2022

Clinical Academic Center of Braga
2022

The current epidemics of type 2 diabetes mellitus (T2DM), non-alcoholic steatohepatitis (NASH), and Alzheimer's disease (AD) all represent insulin-resistance diseases. Previous studies showed that streptozotocin, a nitrosamine-related com-pound, causes insulin resistance diseases including, T2DM, NASH, AD-type neurodegeneration. We hypothesize chronic human exposure to nitrosamine compounds, which are widely present in processed foods, contributes the pathogenesis AD. Long Evans rat pups...

10.3233/jad-2009-1155 article EN Journal of Alzheimer s Disease 2009-10-30

Evidence shows that diabetes increases the risk of developing Alzheimer's disease (AD). Many efforts have been done to elucidate mechanisms linking and AD. To demonstrate mitochondria may represent a functional link between both pathologies, we compared effects AD sucrose-induced metabolic alterations on mouse brain mitochondrial bioenergetics oxidative status. For this purpose, were isolated from wild-type (WT), triple transgenic (3xTg-AD), WT mice fed 20% sucrose-sweetened water for 7...

10.2337/db11-1186 article EN cc-by-nc-nd Diabetes 2012-03-17

Type 2 diabetes (T2D) is considered a major risk factor for Alzheimer's disease (AD). To elucidate the links between both pathological conditions, we compared behavioral and cognitive functions, cerebral amyloid-β peptide (Aβ) levels vasculature integrity of 11-month-old T2D AD mice. For this purpose, performed tests (open field, object recognition, Y-maze, elevated plus maze tests), ELISA to assess plasma markers endothelial/vascular dysfunction, spectrophotometric assays evaluate vascular...

10.3233/jad-130005 article EN Journal of Alzheimer s Disease 2013-05-06

Purpose This study aims to analyze the psychological benefits of digital and paper-based cognitive training in users with a lack technological knowledge low level education. Design/methodology/approach In total, 60 individuals (Mage = 78.38; SDage 9.15) attending day center were recruited complete program, 30 them format. They all assessed on skills, depressive symptomatology before after training. Regardless age, education knowledge, participants completed respective program. Findings The...

10.1108/wwop-12-2024-0083 article EN Working with Older People 2025-02-08

Mitochondria have long been known as the powerhouse of cell. However, these organelles are also pivotal players in neuronal cell death. Mitochondrial dysfunction is a prominent feature chronic brain disorders, including Alzheimer's disease (AD) and Parkinson's (PD), cerebral ischemic stroke. Data derived from morphologic, biochemical, molecular genetic studies indicate that mitochondria constitute convergence point for neurodegeneration. Conversely, implicated neuroprotective signaling...

10.3389/fnagi.2010.00138 article EN cc-by Frontiers in Aging Neuroscience 2010-01-01

Insulin-like growth factor 1 receptor (IGF1R)-mediated signaling pathways modulate important neurophysiological aspects in the central nervous system, including neurogenesis, synaptic plasticity and complex cognitive functions. In present study, we intended to characterize impact of IGF1R deficiency brain, focusing on PI3K/Akt MAPK/ERK1/2 mitochondria-related parameters. For this purpose, used 13-week-old UBC-CreERT2; Igf1rfl/fl male mice which Igf1r was conditionally deleted. caused a...

10.3390/biomedicines9020158 article EN cc-by Biomedicines 2021-02-06
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