A5084803901- Alzheimer's disease research and treatments
- Prion Diseases and Protein Misfolding
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological diseases and metabolism
- Supramolecular Self-Assembly in Materials
- Signaling Pathways in Disease
- Parkinson's Disease Mechanisms and Treatments
- Adenosine and Purinergic Signaling
- Bioactive Compounds in Plants
- Botulinum Toxin and Related Neurological Disorders
- Neurological Disease Mechanisms and Treatments
- Medicinal Plant Research
- S100 Proteins and Annexins
- Trace Elements in Health
- Dementia and Cognitive Impairment Research
- Neurogenesis and neuroplasticity mechanisms
- Computational Drug Discovery Methods
- Cholinesterase and Neurodegenerative Diseases
Baylor College of Medicine
2020-2024
Universidad de Málaga
2019-2023
The University of Texas Health Science Center at Houston
2018-2023
Instituto de Investigación Biomédica de Málaga
2019-2023
Alzheimer's disease (AD) is a devastating neurodegenerative disorder, and there pressing need to identify disease-modifying factors devise interventional strategies. The circadian clock, our intrinsic biological timer, orchestrates various cellular physiological processes including gene expression, sleep, neuroinflammation; conversely, dysfunctions are closely associated with and/or contribute AD hallmarks. We previously reported that the natural compound Nobiletin (NOB) clock-enhancing...
Chronic Wasting Disease (CWD) is a prion disease affecting several cervid species. Among them, white-tailed deer (WTD) are of relevance due to their value in farming and game hunting. The exact events involved CWD transmission captive wild animals still unclear. An unexplored mechanism spread involves transmissions through germplasm, such as semen. Surprisingly, the presence load prions semen male sexual tissues from WTD has not been explored. Here, we described detection bucks utilizing...
Abstract Background The misfolding and deposition of amyloid beta (Aβ) in human brain is the main hallmark Alzheimer's disease (AD) pathology. One drivers Alzheimer´s pathogenesis production soluble oligomeric Aβ, which could potentially serve as a biomarker AD. Methods Given that diphenylalanine (FF) at C‐terminus Aβ fragments plays key role inducing AD pathology, based on hydrophobic structure FF, we synthesized near‐infrared BF2‐dipyrrolmethane fluorescent imaging probe (NB) to detect...
TMEM106B is a risk modifier for growing list of age-associated dementias including Alzheimer’s and frontotemporal dementia, yet its function remains elusive. Two key questions that emerge from past work are whether the conservative T185S coding variant found in minor haplotype contributes to protection, presence helpful or harmful context disease. Here we address both issues while extending testbed study models TDP tauopathy. We show deletion accelerates cognitive decline, hindlimb...
Parkinson's disease (PD) is the second most common neurodegenerative disorder. An important hallmark of PD involves pathological aggregation proteins in structures known as Lewy bodies. The major component these proteinaceous inclusions alpha (α)-synuclein. In different conditions, α-synuclein can assume conformations rich either α-helix or β-sheets. mechanisms misfolding, aggregation, and fibrillation remain unknown, but it thought that β-sheet conformation responsible for its associated...
Abstract Background Current clinical PET imaging relies on translocator protein (TSPO) to detect neuroinflammation in brain disorders including degenerative conditions such as AD, however this marker lacks cell type‐specificity and offers no information what type of insult is causing the reaction. An ideal tracer would both rise pro‐inflammatory loss anti‐inflammatory glial responses discriminate cellular amyloid‐beta from tau. We investigated whether a pair purinergic receptors provide...
Previous works have demonstrated that neuroinflammatory response plays a key role in Alzheimer's disease (AD) progression. Microglia, the main cell type of innate immune system brain, activates both patients and animal models; however, it is still unknown whether this cause or consequence AD. An inefficient immunologic could trigger an increase amyloid-beta levels as progresses. In study, we aimed to investigate effect immunosuppression over pathological progression hippocampus APP/PS1dE9...
Recent evidence suggests that amyloid-beta (Aβ) aggregates present in the brains of Alzheimer's Disease (AD) patients may exist different conformations or “strains”, similarly as observed for infectious prion proteins (PrP). Proof strain variation on misfolded Aβ is found i) fact morphologically synthetic fibrils display variable degrees toxicity (Petkova et al. 2005, Science), ii) existence populations structures clinically diverse subtypes AD (Qiang 2017, Nature), and iii) serial...
Compelling evidence in humans and experimental rodents suggest that Alzheimer's disease (AD) -associated Aβ exists a wide variety of conformational strains. Unfortunately, current research has not addressed the biological significance strain variation AD. This issue acquire additional relevance considering mixtures strains seems to exist brains patients. may explain pathological clinical differences observed among people afflicted by Here, we used two synthetic-Aβ40 (termed 2F 3F) have been...
Abstract Background Currently available treatments for Alzheimer’s disease (AD) are essentially symptomatic and not disease‐modifying, positioning it as a serious global health problem with the increase of elderly population. This is clinically characterized by progressive memory impairment cognitive dysfunction. The neuropathological hallmarks AD accumulation extracellular β‐amyloid (Aβ) peptide in senile plaques, intracellular deposition hyper‐phosphorylated tau neurofibrillary tangles...