A5069233453- Alzheimer's disease research and treatments
- Neuroscience and Neuropharmacology Research
- Diabetes Treatment and Management
- Diet and metabolism studies
- Pancreatic function and diabetes
- Nutritional Studies and Diet
- Metabolomics and Mass Spectrometry Studies
- Neuroinflammation and Neurodegeneration Mechanisms
- Peroxisome Proliferator-Activated Receptors
- Agriculture Sustainability and Environmental Impact
- Nicotinic Acetylcholine Receptors Study
- Diabetes Management and Research
- Neurological Disease Mechanisms and Treatments
- Genetics, Aging, and Longevity in Model Organisms
- Mitochondrial Function and Pathology
- Natural Antidiabetic Agents Studies
- Vagus Nerve Stimulation Research
- Primate Behavior and Ecology
- Suicide and Self-Harm Studies
- Stress Responses and Cortisol
- Insect and Pesticide Research
- Intensive Care Unit Cognitive Disorders
- Down syndrome and intellectual disability research
- Ion channel regulation and function
- Immune cells in cancer
Binghamton University
2025
Wake Forest University
2014-2023
Persistent psychological stress increases the risk of many chronic diseases aging. Little progress has been made to effectively reduce responses or mitigate effects suggesting a need for better understanding factors that influence responses. Limited evidence suggests diet may be factor in modifying stress. However, long-term studies on reactive systems are not available, and controlled randomized clinical trials difficult costly. Here we report outcomes controlled, preclinical trial...
Epidemiological studies identified alcohol use disorder (AUD) as a risk factor for Alzheimer's disease (AD), yet there is conflicting evidence on how promotes AD pathology. In this study, 10-week moderate two-bottle choice drinking paradigm was used to identify chronic ethanol exposure alters amyloid-β (Aβ)-related pathology, metabolism, and behavior. Ethanol-exposed APPswe/PSEN1dE9 (APP/PS1) mice showed increased brain atrophy an number of amyloid plaques. Further analysis revealed that led...
Elevated blood glucose levels, or hyperglycemia, can increase brain excitability and amyloid-β (Aβ) release, offering a mechanistic link between type 2 diabetes Alzheimer's disease (AD). Since the cellular mechanisms governing this relationship are poorly understood, we explored whether ATP-sensitive potassium (KATP) channels, which couple changes in energy availability with excitability, play role AD pathogenesis. First, demonstrate that KATP channel subunits Kir6.2/KCNJ11 SUR1/ABCC8 were...
Epidemiological studies suggest that individuals with type 2 diabetes (T2D) have a twofold to fourfold increased risk for developing Alzheimer's disease (AD), however, the exact mechanisms linking two diseases are unknown. In both conditions, majority of pathophysiological changes, including glucose and insulin dysregulation, resistance, AD-related changes in Aβ tau, occur decades before onset clinical symptoms diagnosis. this study, we investigated relationship between metabolic biomarkers...
Synaptic dysfunction may represent an early and crucial pathophysiology in Alzheimer's disease (AD). Recent studies implicate a connection between synaptic plasticity deficits compromised capacity of de novo protein synthesis AD. The mRNA translational factor eukaryotic elongation 1A (eEF1A) is critically involved several forms long-lasting plasticity. By examining postmortem human brain samples, transgenic mouse model, application synthetic Aβ42 on hippocampal slices, we demonstrated that...
Abstract Currently there is no effective therapy available for cognitive impairments in Down syndrome (DS), one of the most prevalent forms intellectual disability humans associated with chromosomes 21 trisomy. Glucagon-like peptide-1 (GLP-1) an incretin hormone that maintains glucose homeostasis by stimulating insulin secretion. Its natural cleavage product GLP-1 (9-36) lacks insulinotropic effects and has a low binding affinity receptors; thus, historically been identified as inactive...
Glucagon-like peptide-1 (GLP-1) is an endogenous gut hormone and a key regulator in maintaining glucose homeostasis by stimulating insulin secretion. Its natural cleavage product GLP-1 (9-36), used to be considered "bio-inactive" metabolite mainly because of its lack insulinotropic effects low affinity for receptors, possesses unique properties such as anti-oxidant cardiovascular protection. Little known about the role (9-36) central nervous system. Here we report that chronic, systemic...
ABSTRACT Hyperexcitability is a defining feature of Alzheimer’s disease (AD), where aberrant neuronal activity both cause and consequence AD. Therefore, identifying novel targets that modulate cellular excitability an important strategy for treating ATP-sensitive potassium (K ATP ) channels are metabolic sensors excitability. Sulfonylureas K channel antagonists traditionally used to combat hyperglycemia in diabetic patients by inhibiting pancreatic channels, thereby stimulating insulin...
Abstract Epidemiological studies suggest that individuals with type 2 diabetes (T2D) have a 2-4 fold increased risk for developing Alzheimer’s disease (AD), however the exact mechanisms linking two is unknown. In both conditions, majority of pathophysiological changes (including glucose and insulin dysregulation, resistance, AD-related in Aβ tau) occur decades before onset clinical symptoms diagnosis. this study, we investigated relationship between metabolic biomarkers associated T2D...
Abstract Chronic ethanol exposure can increase amyloid-β (Aβ) and tau in rodent models of Alzheimer’s-disease (AD)-like pathology, yet the underlying mechanisms are poorly understood. In this study, a moderate two-bottle choice drinking paradigm was used to identify how chronic alters Aβ-related metabolism, behavior. Complementary vivo microdialysis experiments were measure acute directly modulates Aβ hippocampal interstitial fluid (ISF). Ethanol-exposed APPswe/PSEN1dE9 (APP/PS1) mice showed...
Abstract Persistent psychological stress increases the risk of many chronic diseases aging. Little progress has been made to effectively reduce responses or mitigate effects suggesting a need for better understanding factors that influence responses. Limited evidence suggests diet may be factor in modifying stress. However, long-term studies on reactive systems are not available, and controlled randomized clinical trials difficult costly. Here we report outcomes controlled, preclinical trial...
Brain hyperexcitability is a defining feature of AD, where aberrant neuronal activity may be both cause and consequence the pathology. Identifying novel targets to modulate cellular excitability an important treatment strategy. We showed that inward rectifying, ATP-sensitive potassium (K ATP ) channels regulate at neurovascular unit impact production aggregation amyloid-beta (Aβ), hallmark AD. Sulfonylureas such as glyburide (GLY) are antidiabetic medications inhibit K channels. demonstrated...