A5032194110- Alzheimer's disease research and treatments
- Birth, Development, and Health
- Tryptophan and brain disorders
- Neuroinflammation and Neurodegeneration Mechanisms
- Cholinesterase and Neurodegenerative Diseases
- Diet and metabolism studies
- Neuroscience and Neuropharmacology Research
- Neuroendocrine regulation and behavior
- Parkinson's Disease Mechanisms and Treatments
- Nuclear Receptors and Signaling
- Folate and B Vitamins Research
- Computational Drug Discovery Methods
- Coenzyme Q10 studies and effects
- Infant Nutrition and Health
- Circadian rhythm and melatonin
- Supramolecular Self-Assembly in Materials
- S100 Proteins and Annexins
- Adipose Tissue and Metabolism
- Systemic Sclerosis and Related Diseases
- Antioxidant Activity and Oxidative Stress
- Gut microbiota and health
- Stress Responses and Cortisol
- Biochemical effects in animals
- Immunotherapy and Immune Responses
- Mitochondrial Function and Pathology
Northwestern University
2020-2023
Temple University
2013-2019
Translational Therapeutics (United States)
2016
Thomas Jefferson University
2013
Abstract Impairments in neuronal intracellular calcium ( i Ca 2+ ) handling may contribute to Alzheimer’s disease (AD) development. Metabolic dysfunction and progressive loss are associated with AD progression, mitochondrial m signaling is a key regulator of both these processes. Here, we report remodeling the exchange machinery prefrontal cortex individuals AD. In 3xTg-AD mouse model impaired efflux capacity precedes neuropathology. Neuronal deletion Na + /Ca exchanger (NCLX, Slc8b1 gene)...
Abstract Background Previous studies show that antibiotic-mediated (abx) alteration of the gut microbiome (GMB) results in a reduction amyloid beta (Aβ) plaques and proinflammatory microglial phenotype male APPPS1-21 mice. However, effect GMB perturbation on astrocyte phenotypes microglial-astrocyte communication context amyloidosis has not been examined. Methods To study whether modulates amyloidosis, female mice were treated with broad-spectrum abx leading to perturbation. GFAP +...
Abstract Clinical investigations have highlighted a biological link between reduced brain glucose metabolism and Alzheimer’s disease (AD). Previous studies showed that deprivation may influence amyloid beta formation in vivo but no data are available on the effect this condition might tau protein metabolism. In current paper, we investigated of deficit phosphorylation, memory learning, synaptic function transgenic mouse model tauopathy, h-tau mice. Compared with controls, mice significant...
Environmental stressor exposure is associated with a variety of age-related diseases including neurodegeneration. Although the initial events sporadic Parkinson's disease (PD) are not known, consistent evidence supports hypothesis that results from combined effect genetic and environmental risk factors. Among them, behavioral stress has been shown to cause damage neuronal loss in different areas brain, however, its on dopaminergic system PD pathogenesis remains be characterized. The C57BL/6...
Inflammatory mechanisms have been implicated in Alzheimer's disease (AD) pathogenesis, and among them, the pro-inflammatory 5-lipoxygenase (5LO) enzyme. While previous work has shown that 5LO modulates amyloidotic phenotype of AD, exact metabolic product responsible for this biological action remains unknown. In study, we challenged neuronal cells with leukotriene B4 (LTB4), a major product, found it increased amyloid-β formation whereby elevating steady-state levels γ-secretase proteins,...
FLAP (5-lipoxygenase-activating protein) is a protein widely distributed within the central nervous system whose function to regulate activation of 5-Lipoxygenase enzyme. Although previous works show that pharmacological blockade improve amyloidotic phenotype Tg2576, its contribution tau pathology remains be investigated. In present paper, we studied effect inhibition on metabolism endogenous in these mice. Total levels brains mice receiving MK-591, selective and specific inhibitor, were not...
Abstract Epidemiological studies have suggested a link between exposure to environmental factors early in life and susceptibility neurodegenerative diseases adulthood. In the short term, maternal diet is important for growth development of fetus; however, it may also long‐term effects on health status offspring. Here, we investigate effect that high‐fat during gestation has brain offspring later life. B6129SF2/J dams were fed 3 weeks’ gestation, then switched standard chow after delivery....
Background: Alzheimer’s disease (AD) is initiated by aberrant accumulation of amyloid beta (Aβ) protein in the brain parenchyma. The microenvironment surrounding plaques characterized swelling presynaptic terminals (dystrophic neurites) associated with lysosomal dysfunction, microtubule disruption, and impaired axonal transport. Aβ-induced plasma membrane damage calcium influx could be potential mechanisms underlying dystrophic neurite formation. Objective: We tested whether promoting...
Alzheimer's disease (AD) is the leading cause of dementia, afflicting 5 million Americans and costing over 200 billion dollars per year. The mechanisms involved in AD pathogenesis are still poorly understood. Moreover, no therapy available to cure or slow down its progression. study new pathways necessary develop therapeutic targets. 12/15-lipoxygenase enzymatic pathway (12/15-LO) upregulated postmortem brain tissues cerebrospinal fluid patients. Its genetic absence pharmacological...
Together with aging, a family history for Alzheimer's disease (AD) is considered strong risk factor developing the late-onset form of disease. Studies have shown that subjects having mother affected by are at higher to develop AD later in life compared subject father AD. While no genetic factors been identified, lifestyle and nutrition emerged as possible mediators. Interestingly, evidence showed high sugar (HS) diet directly influences development AD-like phenotype, however, whether this...
The identification of risk factors for sporadic late-onset Alzheimer's disease (AD) is important because it can provide mechanistic, diagnostic and therapeutic clues into this chronic neurodegenerative disorder. A family history AD increases the to develop disease, a maternal influences more than paternal one. While dietary lifestyle and, in particular, direct exposure high cholesterol saturated fat diet known modulate many aspect phenotype, no information available on impact that factor has...