A5043937248- Alzheimer's disease research and treatments
- Intracerebral and Subarachnoid Hemorrhage Research
- Neuroinflammation and Neurodegeneration Mechanisms
- Neurological Disease Mechanisms and Treatments
- Dementia and Cognitive Impairment Research
- Sleep and Wakefulness Research
- Cannabis and Cannabinoid Research
- Neuroscience and Neuropharmacology Research
- S100 Proteins and Annexins
- Amyloidosis: Diagnosis, Treatment, Outcomes
- Neurological Disorders and Treatments
- Immune cells in cancer
- Cholinesterase and Neurodegenerative Diseases
- GABA and Rice Research
- Neuroscience of respiration and sleep
- Tryptophan and brain disorders
Eli Lilly (United States)
2022-2024
Indiana University – Purdue University Indianapolis
2019-2022
Indiana University School of Medicine
2019-2022
Indiana University Bloomington
2019
Abstract Tau aggregation is a defining histopathological feature of Alzheimer’s disease and other tauopathies. However, the cellular mechanisms involved in tau propagation remain unclear. Here, we performed an unbiased quantitative proteomic study to identify proteins that specifically interact with this seed. We identified Bassoon (BSN), presynaptic scaffolding protein, as interactor seed isolated from mouse model tauopathy, progressive supranuclear palsy postmortem samples. show BSN...
Amyloid-related imaging abnormalities (ARIA) have been identified as the most common and serious adverse events resulting from pathological changes in cerebral vasculature during several recent anti-amyloid-β (Aβ) immunotherapy trials. However, precise cellular molecular mechanisms underlying how amyloid enhances angiopathy (CAA)-mediated alterations vascular permeability microhemorrhages are not currently understood. Interestingly, brain perivascular macrophages implicated regulating CAA...
Abstract Background Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. The mechanisms underlying contribution CAA to neurodegeneration are not currently understood. Although highly associated with accumulation beta (Aβ), other amyloids known associate vasculature. Alzheimer’s disease (AD) characterized parenchymal Aβ deposition, intracellular tau, and significant neuroinflammation. increases age present in 85–95% individuals AD. A substantial amount...
Abstract Reactive astrogliosis is a universal response of astrocytes to abnormal events and injuries. Studies have shown that proinflammatory microglia can polarize (designated A1 astrocytes) toward neurotoxic phenotype characterized by increased Complement Component 3 (C3) expression. It still unclear if inflammatory stimuli from other cell types may also be capable inducing subset C3 + astrocytes. Here, we show subtype induced activated endothelial cells distinct microglia. Furthermore,...
Pathological aggregation of tau and neuroinflammatory changes mark the clinical course Alzheimer's disease related tauopathies. To understand correlation between these pathological hallmarks functional deficits, we assessed behavioral physiological deficits in PS19 mouse model, a broadly utilized model tauopathy. At 9 months, mice have characteristic hyperactive behavior, decline motor strength, deterioration conditions marked by lower body temperature, reduced weight, an increase measures...
Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. Currently, there no clear understanding mechanisms underlying contribution CAA to neurodegeneration. Despite fact that highly associated with accumulation Aβ, other types amyloids have been shown associate vasculature. Interestingly, in many cases, vascular amyloidosis accompanied significant tau pathology. However, neurodegeneration remains be determined. We used a mouse model Familial Danish...
We previously showed that cannabinoid-related GPR18 receptors are present in the murine corneal epithelium, but their function remains unknown. The related CB1 regulate healing, possibly via chemotaxis. therefore examined a potential role for epithelial chemotaxis and wound healing.
Abstract Background Anti-amyloid-β (Aβ) immunotherapy trials have revealed amyloid-related imaging abnormalities (ARIA) as the most prevalent and serious adverse events linked to pathological changes in cerebral vasculature. Recent studies underscore critical involvement of perivascular macrophages infiltration peripheral immune cells regulating cerebrovascular damage. Specifically, Aβ antibodies engaged at amyloid angiopathy (CAA) deposits trigger macrophage activation upregulation genes...
ABSTRACT Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. The mechanisms underlying contribution CAA to neurodegeneration are not currently understood. Although highly associated with accumulation β‐amyloid (Aβ), other amyloids known associate vasculature. Alzheimer's disease (AD) characterized parenchymal Aβ and intracellular tau as neurofibrillary tangles (NFTs), affecting synapses directly, leading behavioral physical impairment. increases age...
Alzheimer's disease is a neurological disorder characterized by the overproduction and aggregation of amyloid-beta phosphorylation intraneuronal accumulation tau. These events promote synaptic dysfunction loss, leading to neurodegeneration cognitive deficits. Astrocytes are intimately associated with synapses become activated under pathological conditions, becoming neurotoxic detrimentally affecting synapses. Although it has been established that reducing neuronal tau expression prevents...
Abstract Background Anti‐amyloid‐β (Aβ) immunotherapy trials have shown amyloid‐related imaging abnormalities (ARIA) as the most common and serious adverse events linked to pathological changes in cerebral vasculature. Nevertheless, mechanisms underlying how amyloid triggers vascular damage, increases permeability, results microhemorrhages remains unclear. Notably, activation of perivascular macrophages infiltration peripheral immune cells been implicated regulating cerebrovascular damage....
Abstract Background Amyloid‐related imaging abnormalities (ARIA) have been identified as the most common and serious adverse events caused by pathological changes in cerebral vasculature during several recent anti‐amyloid‐b (Aß) immunotherapy trials. However, cellular molecular mechanisms underlying how amyloid enhances angiopathy (CAA)‐mediated alterations of vascular permeability microhemorrhages are not currently understood. Interestingly, brain perivascular macrophages implicated...
Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. Currently, there no clear understanding mechanisms underlying contribution CAA to neurodegeneration. Despite fact that highly associated with accumulation Aβ, other types amyloids have been shown associate vasculature. Interestingly, in many cases, vascular amyloidosis accompanied significant tau pathology. However, neurodegeneration remains be determined. We used a mouse model Familial Danish...