A5088970359- Neuroscience and Neuropharmacology Research
- Alzheimer's disease research and treatments
- Ion channel regulation and function
- Receptor Mechanisms and Signaling
- Memory and Neural Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Pharmacological Receptor Mechanisms and Effects
- Dementia and Cognitive Impairment Research
- Nicotinic Acetylcholine Receptors Study
- Pain Mechanisms and Treatments
- Cholinesterase and Neurodegenerative Diseases
- Liver Disease Diagnosis and Treatment
- Neuropeptides and Animal Physiology
- Neuroscience and Neural Engineering
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Apelin-related biomedical research
- Trace Elements in Health
- Vitamin K Research Studies
- Glutathione Transferases and Polymorphisms
- Mitochondrial Function and Pathology
- Metabolism and Genetic Disorders
University of Castilla-La Mancha
2019-2025
Instituto de Neurociencias
2018-2022
Biomedical Research Networking Center on Neurodegenerative Diseases
2018-2022
Hippocampal synaptic plasticity disruption by amyloid-β (Aβ) peptides + thought to be responsible for learning and memory impairments in Alzheimer's disease (AD) early stage. Failures neuronal excitability maintenance seems an underlying mechanism. G-protein-gated inwardly rectifying potassium (GirK) channels control neural hyperpolarization response many G-protein-coupled receptors activation. Here, vitro vivo amyloidosis mouse models, we study whether GirK take part of the hippocampal...
The G-protein-gated inwardly rectifying potassium (Kir3/GIRK) channel is the effector of many G-protein-coupled receptors (GPCRs). Its dysfunction has been linked to pathophysiology Down syndrome, Alzheimer9s and Parkinson9s diseases, psychiatric disorders, epilepsy, drug addiction, or alcoholism. In hippocampus, GIRK channels decrease excitability cells contribute resting membrane potential inhibitory neurotransmission. Here, elucidate role activity in maintenance hippocampal-dependent...
The amyloid-β (Aβ) cascade is one of the most studied theories linked to AD. In multiple models, Aβ accumulation and dyshomeostasis have shown a key role in AD onset, leading excitatory/inhibitory imbalance, impairments synaptic plasticity oscillatory activity, memory deficits. Despite higher prevalence Alzheimer's disease (AD) women compared men, possible sex difference scarcely explored information from amyloidosis transgenic mice models contradictory. Thus, given lack data regarding early...
In early Alzheimer disease (AD) models synaptic failures and upstreaming aberrant patterns of network synchronous activity result in hippocampal-dependent memory deficits. such initial stage, soluble forms Amyloid-β (Aβ) peptides have been shown to play a causal role. Among different Aβ species, Aβ25–35 has identified as the biologically active fragment, induces major neuropathological signs related AD stages. Consequently, it extensively used acutely explore pathophysiological events with...
Abstract Carnitine palmitoyltransferase 1c (CPT1C) is a neuron‐specific protein widely distributed throughout the CNS and highly expressed in discrete brain areas including hypothalamus, hippocampus, amygdala different motor regions. Its deficiency has recently been shown to disrupt dendritic spine maturation AMPA receptor synthesis trafficking but its contribution synaptic plasticity cognitive learning memory processes remains mostly unknown. Here, we aimed explore molecular, synaptic,...
Reelin binds to the apolipoprotein E receptor apoER2 activate an intracellular signaling cascade. The proteolytic cleavage of reelin follows binding but can also occur independently its receptors. This study assesses whether fragments are differentially affected in cerebrospinal fluid (CSF) Alzheimer’s disease (AD) subjects. CSF species were analyzed by Western blotting, employing antibodies against N- and C-terminal domains. In AD patients, we found a decrease 420 kDa full-length compared...
Abstract Sigma-1 receptors (S1Rs) are widely expressed throughout the central nervous system and modulate neuron intracellular calcium levels, leading to changes in neurotransmitter release neuronal activity. They also interact with various proteins signaling pathways, playing a key role regulating synaptic plasticity brain areas such as hippocampus, thereby influencing learning memory processes. This opens research avenue explore S1R modulation potential therapeutic target diseases...
Abstract Background : In early stages of Alzheimer's disease (AD), soluble amyloid- β (A ) is a key player disrupting neuronal activity and contributing to cognitive decline in advanced the disease. While hippocampus has been central focus prior research due its susceptibility A -induced alterations, comprehensive understanding AD pathology requires exploring interconnected brain regions. The posterior parietal cortex (PPC), collaborating closely with involved various memory processes,...
Abstract G-protein-gated inwardly rectifying potassium (Kir3/GirK) channel is the effector of many G-protein-coupled receptors. Its dysfunction has been linked to pathophysiology Down syndrome, Alzheimer’s and Parkinson’s diseases, psychiatric disorders, epilepsy, drug addiction, or alcoholism. GirK channels are constitutively activated in dorsal hippocampus contributing resting membrane potential, their synaptic activation compensates any excitation excess. Here, order elucidate role...
Abstract Background Hippocampal synaptic plasticity disruption by amyloid‐ β (A ) peptides is thought to be responsible for learning and memory impairments in Alzheimer's disease (AD) early stage. Failures neuronal excitability maintenance seems an underlying mechanism. G‐protein‐gated inwardly‐rectifying potassium (GirK) channels control neural hyperpolarization response many G‐protein‐coupled receptors activation. Method Here, vitro vivo amyloidosis mouse models, we study whether GirK take...
Abstract Background One of the neuropathological hallmarks Alzheimer’s disease (AD) is amyloid- β (A ) accumulation in hippocampus that causes its dysfunction. This disruption includes excitatory/inhibitory imbalance, synaptic plasticity and oscillatory activity impairments, memory deficits. Although AD prevalence higher women than men, possible sex difference scarcely explored information from amyloidosis transgenic mice models contradictory. Thus, given lack data early stages females, aim...
Abstract Background In early stages of Alzheimer’s disease, disruption learning and memory processes that rely on hippocampal performance correlates with aberrant patterns synchronous neuronal activity arise prior to evident neurodegeneration. These disturbances emerge as a result hyperexcitability synaptic dysfunction induced by soluble forms amyloid‐ β (A ) peptide, which trigger an imbalance between excitatory inhibitory neurotransmission systems. The molecular mechanisms underlying these...