A5001982801- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disease Mechanisms and Treatments
- Computational Drug Discovery Methods
- Nuclear Receptors and Signaling
- Microtubule and mitosis dynamics
- Cholinesterase and Neurodegenerative Diseases
- Prion Diseases and Protein Misfolding
- Tryptophan and brain disorders
- Advanced Glycation End Products research
- Medicinal Plants and Neuroprotection
- Advanced Neuroimaging Techniques and Applications
- Neurogenesis and neuroplasticity mechanisms
- Ginkgo biloba and Cashew Applications
- Pluripotent Stem Cells Research
- Agriculture and Biological Studies
- Immune cells in cancer
- Mitochondrial Function and Pathology
- Agriculture, Plant Science, Crop Management
- Genetics, Bioinformatics, and Biomedical Research
- Biological Research and Disease Studies
- Nanoplatforms for cancer theranostics
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Neuroscience and Neuropharmacology Research
- Barrier Structure and Function Studies
Universidad de Málaga
2016-2025
Instituto de Investigación Biomédica de Málaga
2016-2025
Biomedical Research Networking Center on Neurodegenerative Diseases
2017-2025
Instituto de Salud Carlos III
2025
Lund University
2022-2024
Bridge University
2023
Netherlands Institute for Neuroscience
2023
Reactive astrogliosis, a complex process characterized by cell hypertrophy and upregulation of components intermediate filaments, is common feature in brains Alzheimer's patients. astrocytes are found close association with neuritic plaques; however, the precise role these glial cells disease pathogenesis unknown. In this study, using immunohistochemical techniques light electron microscopy, we report that plaque-associated reactive enwrap, engulf may digest presynaptic dystrophies...
The role of microglial cells in the development and progression Alzheimer's disease (AD) has not been elucidated. Here, we demonstrated existence a weak response human AD hippocampus which is contrast to massive activation observed APP-based models. Most importantly, displayed prominent degenerative profile (dentate gyrus > CA3 CA1 parahippocampal gyrus), including fragmented dystrophic processes with spheroids, reduced numerical density, significant decrease area surveillance ("microglial...
Abstract The majority of Alzheimer’s disease (AD) cases are late-onset and occur sporadically, however most mouse models the harbor pathogenic mutations, rendering them better representations familial autosomal-dominant forms disease. Here, we generated knock-in mice that express wildtype human Aβ under control App locus. Remarkably, changing 3 amino acids in sequence to its wild-type counterpart leads age-dependent impairments cognition synaptic plasticity, brain volumetric changes,...
Abstract Background Amyloid beta (Aβ) deposits and hyperphosphorylated tau (p-tau) accumulation have been identified in the retina of Alzheimer’s disease (AD) patients transgenic AD mice. Previous studies shown that retinal microglia engulf Aβ, but this property decreases patients. Whether also take up p-tau if event is affected yet not described. In current study, we use p-tau-specific thiophene-based ligand bTVBT2 to investigate relationship between progression uptake by App NL−F/NL−F...
Abstract Reactive astrocytes and dystrophic neurites, most aberrant presynaptic elements, are found surrounding amyloid‐β plaques in Alzheimer's disease (AD). We have previously shown that reactive enwrap, phagocytose, degrade synapses the hippocampus of APP mice AD patients, but affecting less than 7% suggesting reduced phagocytic capacity AD. Here, we aimed to gain insight into underlying mechanisms by analyzing primary astrocyte cultures phagocytose isolated (synaptoneurosomes, SNs) from...
Neuronal loss is the best neuropathological substrate that correlates with cortical atrophy and dementia in Alzheimer's disease (AD). Defective GABAergic neuronal functions may lead to network hyperactivity aberrant oscillations consequence, generate a detrimental alteration memory processes. In this study, using immunohistochemical stereological approaches, we report two major non-overlapping groups of inhibitory interneurons (SOM-cells PV-cells) displayed distinct vulnerability perirhinal...
Abstract In Alzheimer’s disease (AD), and other tauopathies, microtubule destabilization compromises axonal synaptic integrity contributing to neurodegeneration. These diseases are characterized by the intracellular accumulation of hyperphosphorylated tau leading neurofibrillary pathology. AD brains also accumulate amyloid-beta (Aβ) deposits. However, effect stabilizing agents on Aβ pathology has not been assessed so far. Here we have evaluated impact brain-penetrant microtubule-stabilizing...
ABSTRACT Alzheimer's disease (AD) is a complex neurodegenerative proteinopathy in which Aβ and tau misfold aggregate into entities that structurally unsettle native proteins, mimicking prion‐like or “seeding” process. These “seeds” can arrange different conformations strains might display distinct pathogenic properties. Furthermore, recent evidence suggests microglia play key role the amyloidogenic event modulate propagation aggregation processes. Here, we employed histological molecular...
Abstract Background Alzheimer’s disease (AD) is foremost characterized by β-amyloid (Aβ)-extracellular plaques, tau-intraneuronal fibrillary tangles (NFT), and neuroinflammation, but over the last years it has become evident that peripheral inflammation might also contribute to disease. AD patients often demonstrate increased levels of circulating proinflammatory mediators altered antibody in blood. In our study, we investigated plasma Immunoglobulin A (IgA) association with apolipoprotein E...
Abstract The islet amyloid polypeptide (IAPP), a pancreas-produced peptide, has beneficial functions in its monomeric form. However, IAPP aggregates, related to type 2 diabetes mellitus (T2DM), are toxic not only for the pancreas, but also brain. In latter, is often found vessels, where it highly pericytes, mural cells that have contractile properties and regulate capillary blood flow. current study, we use microvasculature model, human brain vascular pericytes (HBVP) co-cultured together...
Pancreas-derived islet amyloid polypeptide (IAPP) crosses the blood-brain barrier and co-deposits with beta (Aβ) in brains of type 2 diabetes (T2D) Alzheimer's disease (AD) patients. Depositions might be related to circulating IAPP levels, but it warrants further investigation. Autoantibodies recognizing toxic oligomers (IAPPO) not monomers (IAPPM) or fibrils have been found T2D, studies on AD are lacking. In this study, we analyzed plasma from two cohorts that levels neither immunoglobulin...
Abstract Background Alzheimer’s Disease (AD) is a neurodegenerative proteinopathy in which Aβ can misfold and aggregate into seeds that structurally corrupt native proteins, mimicking prion‐like process. These amyloid aggregation propagation processes are influenced by three factors: the origin of seed, time incubation host. However, mechanism underlying differential effect each factor poorly known. Previous studies have shown source relevant for process, since its pathogenicity different...
Abstract Background Most age‐associated neurodegenerative disorders involve the aggregation of specific proteins within nervous system, as occurs in Alzheimer’s disease (AD). Recent evidence indicates that Aβ can misfold and aggregate into seeds structurally corrupt native proteins, mimicking a prion‐like process template protein corruption or seeding. In fact, studies FAD‐based animal models show deposition cerebral amyloid angiopathy may be induced by intracerebral infusion brain extracts...
Abstract Background Most age‐associated neurodegenerative disorders involve the aggregation of specific proteins within nervous system, as occurs in Alzheimer’s disease (AD). Recent evidence indicates that Aβ can misfold and aggregate into seeds structurally corrupt native proteins, mimicking a prion‐like process template protein corruption or seeding. In fact, studies animal models show injection brain homogenates from AD patients aged APP‐transgenic mice containing aggregates, induce some...
Abstract Background: Amyloid beta (Ab) deposits and hyperphosphorylated tau (p-tau) accumulation have been identified in the retina of Alzheimer’s disease (AD) patients transgenic AD mice. Previous studies shown that retinal microglia engulf Ab, but this property decrease patients. Whether also take up p-tau if event is affected yet not described. In current study, we use specific thiophene-based ligand bTVBT2 to investigate relationship between progression uptake App NL-F/NL-F knock-in...
Abstract Background Alzheimer’s Disease (AD) is a neurodegenerative proteinopathy in which Aβ can misfold and aggregate into seeds that structurally corrupt native proteins, mimicking prion‐like process. These amyloid aggregation propagation processes are influenced by three factors: the origin of seed, time incubation host. However, mechanism underlying differential effect each factor poorly known. Previous studies have shown source relevant for process, since its pathogenicity different...