A5074978554- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Sirtuins and Resveratrol in Medicine
- Adipose Tissue and Metabolism
- Biochemical effects in animals
- Mitochondrial Function and Pathology
- Cholinesterase and Neurodegenerative Diseases
- Cancer-related Molecular Pathways
- Tryptophan and brain disorders
- Epigenetics and DNA Methylation
- Cell death mechanisms and regulation
- Genetics, Aging, and Longevity in Model Organisms
- Nuclear Receptors and Signaling
- Neurogenesis and neuroplasticity mechanisms
- Eicosanoids and Hypertension Pharmacology
- Higher Education Teaching and Evaluation
- Diet and metabolism studies
- Stress Responses and Cortisol
- Circadian rhythm and melatonin
- DNA Repair Mechanisms
- X-ray Diffraction in Crystallography
- Crystallization and Solubility Studies
- Histone Deacetylase Inhibitors Research
- Genetics and Neurodevelopmental Disorders
Universitat de Barcelona
2016-2025
Biomedical Research Networking Center on Neurodegenerative Diseases
2014-2025
Instituto de Salud Carlos III
2007-2025
Centro de Investigación Biomédica en Red
2008-2023
Institut de Biomedicina de la Universitat de Barcelona
2007-2021
Instituto de Neurociencias
2017
Universitat de València
2015
Instituto Nacional de Neurología y Neurocirugía
2014
Universitat Autònoma de Barcelona
2008-2012
Weatherford College
2010-2012
A novel series of donepezil−tacrine hybrids designed to simultaneously interact with the active, peripheral and midgorge binding sites acetylcholinesterase (AChE) have been synthesized tested for their ability inhibit AChE, butyrylcholinesterase (BChE), AChE-induced Aβ aggregation. These compounds consist a unit tacrine or 6-chlorotacrine, which occupies same position as at AChE active site, 5,6-dimethoxy-2-[(4-piperidinyl)methyl]-1-indanone moiety donepezil (or indane derivative thereof),...
The amyloid-β protein precursor/presenilin 1 (AβPP/PS1) mouse model of Alzheimer's disease (AD) has provided robust neuropathological hallmarks familial AD-like pattern. AD is a neurodegenerative process that causes severe cognitive impairment; it
Late-onset Alzheimer's disease (AD) is the most common form of AD appearing after 65 years age. To date, however, there are no non-genetically manipulated rodent models that develop a similar sporadic onset with age-related amyloid-beta (Abeta) deposition. Although senescence accelerated mouse prone 8 (SAMP8) mice have been proposed as model AD, presence Abeta deposits remains controversial. In this study, we describe time course deposition in SAMP8 well control SAMR1 and ICR-CD1 strains...
Aging is accompanied by a decline in memory and other brain functions. Physical exercise may mitigate this through the modulation of factors participating crosstalk between skeletal muscle brain, such as neurotrophins oxidative stress parameters. We aimed to determine whether long term training (35 ± 15 years) promotes maintenance middle-aged men, characterize changes neurotrophic lipid oxidation markers peripheral blood samples both young men. The neuropsychological analysis showed...
5XFAD is an early-onset mouse transgenic model of Alzheimer disease (AD). Up to now there are no studies that focus on the epigenetic changes produced as a result Aβ-42 accumulation and possible involvement in different expression related AD-genes. Under several behavioral cognition test, we found impairment memory psychoemotional female mice reference wild type worsens with age.Cognitive correlated alterations protein level analysis gene markers tau aberrant phosphorylation, amyloidogenic...
Oxidative damage is involved in the pathophysiology of age-related ailments, including Alzheimer's disease (AD). Studies have shown that brain tissue and also lymphocytes from AD patients present increased oxidative stress compared to healthy controls (HCs). Here, we use lymphoblastoid cell lines (LCLs) HCs investigate role resveratrol (RV) selenium (Se) reduction reactive oxygen species (ROS) generated after an injury. We studied whether these compounds elicited expression changes genes...
Cumulative evidence shows that modifications in lifestyle factors constitute an effective strategy to modulate molecular events related neurodegenerative diseases, confirming the relevant role of epigenetics. Accordingly, Environmental Enrichment (EE) represents approach ameliorate cognitive decline and neuroprotection Alzheimer's disease (AD). AD is characterized by specific neuropathological hallmarks, such as β-amyloid plaques Neurofibrillary Tangles, which severely affect areas brain...
Fatty acids play prominent roles in brain function as they participate structural, metabolic and signaling processes. The homeostasis of fatty related pathways is known to be impaired cognitive decline dementia, but the relationship between these disturbances common risk factors, namely ɛ4 allele apolipoprotein E (ApoE-ɛ4) gene sex, remains elusive.In order investigate early alterations associated with acid-related serum metabolome, we here applied targeted metabolomics analysis on a nested...
With innumerable clinical failures of target-specific drug candidates for multifactorial diseases, such as Alzheimer's disease (AD), which remains inefficiently treated, the advent multitarget discovery has brought a new breath hope. Here, we disclose class 6-chlorotacrine (huprine)-TPPU hybrids dual inhibitors enzymes soluble epoxide hydrolase (sEH) and acetylcholinesterase (AChE), profile to provide cumulative effects against neuroinflammation memory impairment. Computational studies...