A5076924297- Neuroinflammation and Neurodegeneration Mechanisms
- Neuroscience and Neuropharmacology Research
- Estrogen and related hormone effects
- Tryptophan and brain disorders
- Reproductive Physiology in Livestock
- Menopause: Health Impacts and Treatments
- Stress Responses and Cortisol
- Genetics and Neurodevelopmental Disorders
- Circadian rhythm and melatonin
- Memory and Neural Mechanisms
- Neurogenesis and neuroplasticity mechanisms
- Crop Yield and Soil Fertility
- Fish Ecology and Management Studies
- Cancer-related cognitive impairment studies
- Liver Disease Diagnosis and Treatment
- Diet and metabolism studies
- Alzheimer's disease research and treatments
- Epigenetics and DNA Methylation
- Retinal Development and Disorders
- Genomics, phytochemicals, and oxidative stress
- Bee Products Chemical Analysis
- Intensive Care Unit Cognitive Disorders
- Anesthesia and Neurotoxicity Research
- Adipose Tissue and Metabolism
- Redox biology and oxidative stress
Maharishi Markandeshwar University, Mullana
2025
Central Institute for Research on Goats
2025
Indian Council of Agricultural Research
2014-2025
University of Florida
2015-2024
Central Sheep and Wool Research Institute
2019-2024
Rajasthan University of Veterinary and Animal Sciences
2019-2024
Santosh University
2024
University of Ottawa
1999-2023
National Bureau of Plant Genetic Resources
2022
Florida College
2009-2020
Retinal pigment epithelium-specific protein 65 kDa (RPE65) is a responsible for isomerization of all-trans-retinaldehyde to its photoactive 11-cis-retinaldehyde and essential the visual cycle. RPE65 mutations can cause severe, early onset retinal diseases such as Leber congenital amaurosis (LCA). A naturally occurring rodent model LCA with recessive nonsense Rpe65 mutation, rd12 mouse, displays profoundly diminished rod electroretinogram (ERG), an absence rhodopsin, overaccumulation retinyl...
Abstract We examine similar and differential effects of two senolytic treatments, ABT‐263 dasatinib + quercetin (D Q), in preserving cognition, markers peripheral senescence, brain aging thought to underlie cognitive decline. Male F344 rats were treated from 12 18 months age with D Q, ABT‐263, or vehicle, compared young (6 months). Both treatments rescued memory, preserved the blood–brain barrier (BBB) integrity, prevented age‐related decline hippocampal N‐methyl‐D‐aspartate receptor (NMDAR)...
Abstract Doxorubicin (Dox), a widely used treatment for cancer, can result in chemotherapy‐induced cognitive impairments (chemobrain). Chemobrain is associated with inflammation and oxidative stress similar to aging. As such, Dox has also been as model of However, it unclear if induces brain changes that observed during aging since does not readily enter the brain. Rather, mechanism chemobrain likely involves induction peripheral cellular senescence release senescence‐associated secretory...
purpose. To test AAV-mediated gene therapy in the rd10 mouse, a natural model of recessive RP caused by mutation β-subunit rod photoreceptor cGMP phosphodiesterase. methods. One eye cohort mice kept dark environment was subretinally injected at postnatal day (P) 14 with 1 μL AAV5-smCBA-PDEβ. The contralateral not injected. animals were then maintained for 2 weeks before they moved to normal 12-hour light/12-hour cycling light visually guided behavioral training. Three after injection,...
Estradiol rapidly modulates hippocampal synaptic plasticity and transmission; however, the contribution of various estrogen receptors to rapid changes in function is unclear. This study examined effect receptor selective agonists on transmission slices obtained from 3–5-month-old wild type (WT), alpha (ERαKO), beta (ERβKO) knockout female ovariectomized mice. Hippocampal were prepared 10–16 days following ovariectomy extracellular excitatory postsynaptic field potentials recorded CA3-CA1...
The expression of the ERα and ERβ estrogen receptors in hippocampus may be important etiology age-related cognitive decline. To examine role regulating transcription learning, ovariectomized wild-type (WT) knockout (KO) mice were used. Hippocampal gene young ERαKO was similar to WT 6 h after a single estradiol treatment. In middle-age mice, hormone deprivation associated with decrease select genes blood-brain barrier; cyclic treatment increased these improved learning mice. contrast ERβKO...
Histone deacetylase (HDAC) inhibitors may have therapeutic utility in multiple neurological and psychiatric disorders, but the underlying mechanisms remain unclear. Here, we identify BRD4, a BET bromodomain reader of acetyl-lysine histones, as an essential component involved potentiated expression brain-derived neurotrophic factor (BDNF) memory following HDAC inhibition. In vitro studies, reveal that pharmacological inhibition BRD4 reversed increase BDNF mRNA induced by class I/IIb inhibitor...
There are sex differences in vulnerability and resilience to the stressors of aging subsequent age-related cognitive decline. Cellular senescence occurs as a response damaging or stress-inducing stimuli. The includes state irreversible growth arrest, development senescence-associated secretory phenotype, release pro-inflammatory cytokines associated with diseases. Senolytics compounds designed eliminate senescent cells. Our recent work indicates that senolytic treatment preserves function...
A decrease in the excitability of CA1 pyramidal neurons contributes to age related hippocampal function and memory decline. Decreased neuronal aged can be observed as an increase Ca(2+)- activated K(+)- mediated post burst afterhyperpolarization (AHP). In this study, we demonstrate that slow component AHP (sAHP) (aged-sAHP) is decreased ∼50% by application reducing agent dithiothreitol (DTT). The DTT-mediated sAHP was specific, such it (20-25 mo), but not young (6-9 mo) F344 rats. effect DTT...
The current study investigates DNA methylation as a possible epigenetic regulator of transcription associated with aging and cognitive function. Young aged male Fischer 344 rats were behaviorally characterized on set shifting task, whole genome bisulfite sequencing was employed to profile the methylome medial prefrontal cortex (mPFC). also compared RNA expression in mPFC from same animals. Variability mainly observed for CpG sites opposed CHG CHH sites. Gene bodies, specifically introns,...
A decline in estradiol (E2)-mediated cognitive benefits denotes a critical window for the therapeutic effects of E2, but mechanism closing is unknown. We hypothesized that upregulating expression estrogen receptor α (ERα) or β (ERβ) hippocampus aged animals would restore potential E2 treatments and rejuvenate E2-induced hippocampal plasticity. Female rats (15 months) were ovariectomized, and, 14 weeks later, adeno-associated viral vectors used to express ERα, ERβ, green fluorescent protein...
Cognitive function depends on transcription; however, there is little information linking altered gene expression to impaired prefrontal cortex during aging. Young and aged F344 rats were characterized attentional set shift spatial memory tasks. Transcriptional differences associated with age cognition examined using RNA sequencing construct transcriptomic profiles for the medial (mPFC), white matter, region CA1 of hippocampus. The results indicate regional in vulnerability Age-related mPFC...
The current study employed next-generation RNA sequencing to examine gene expression differences related brain aging, cognitive decline, and hippocampal subfields. Young aged rats were trained on a spatial episodic memory task. Hippocampal regions CA1, CA3, the dentate gyrus isolated. Poly-A mRNA was examined using two different platforms, Illumina, Ion Proton. Illumina platform used generate seed lists of genes that statistically differentially expressed across regions, ages, or in...
Cisplatin is one of the most widely used chemotherapeutic drugs for treatment cancer. Unfortunately, its major side effects permanent hearing loss. Here, we show that glutathione transferase α4 (GSTA4), a member Phase II detoxifying enzyme superfamily, mediates reduction cisplatin ototoxicity by removing 4-hydroxynonenal (4-HNE) in inner ears female mice. Under treatment, loss Gsta4 results more profound mice compared to male stimulates GSTA4 activity ear wild-type, but not wild-type In...
During aging humans lose midbrain dopamine neurons, but not all regions exhibit vulnerability to neurodegeneration. Microglia maintain tissue homeostasis and neuronal support, microglia become senescent likely some of their functional abilities. Since is the greatest risk factor for Parkinson's disease, we hypothesized that aging-related changes in neurons occur vulnerable substantia nigra pars compacta (SNc) ventral tegmental area (VTA). We conducted stereological analyses enumerate...