25 results for “Cerebrovascular Neurodegeneration”. Showing 25 of 39,449.
Epidemiology of Vascular Dementia.
neurodegeneration. Cerebrovascular disease will be present in most individuals with
FoxO1-miRNA interacting networks as potential targets for mitochondrial diseases.
neurodegeneration, cerebrovascular, and cardiovascular disease. For cardiovascular tissue, which relies
An Engineered Adeno-Associated Virus Capsid Mediates Efficient Transduction of Pericytes and Smooth Muscle Cells of the Brain Vasculature.
Neurodegeneration and cerebrovascular disease share an underlying microvascular dysfunction that
Reconstruction of the Blood-Brain Barrier In Vitro to Model and Therapeutically Target Neurological Disease.
cerebrovascular disease and neurodegeneration, to investigate how genetics and lifestyle
Impact of Helicobacter pylori and metabolic syndrome on mast cell activation-related pathophysiology and neurodegeneration.
cerebrovascular and neurodegenerative disorders. Meningeal MC can be activated by triggers including stress and toxins resulting in vascular changes and neurodegeneration
GLUT1 reductions exacerbate Alzheimer's disease vasculo-neuronal dysfunction and degeneration.
neurodegeneration that develop after initial cerebrovascular degenerative changes. We also
Fibrinogen Induces Microglia-Mediated Spine Elimination and Cognitive Impairment in an Alzheimer's Disease Model.
cerebrovascular damage with immune-mediated neurodegeneration and may have important
Brain macrophages in vascular health and dysfunction.
progression of cerebrovascular diseases, as seen in vessel-associated neurodegeneration.
Monocyte-derived IL-6 programs microglia to rebuild damaged brain vasculature.
Cerebrovascular injury (CVI) is a common pathology caused by infections, injury, stroke, neurodegeneration
Cerebrovascular Unit Activation and Response Following Traumatic Brain Injury.
neurodegeneration, leading to various neurologic and psychiatric disorders. This review examines the cerebrovascular
Unravelling the therapeutic potential of chrysin against ischemic stroke and post-stroke cognitive impairment: a network pharmacology and in-silico perspective.
cerebrovascular disorder that, if left untreated, can lead to secondary neurodegeneration
A1 reactive astrocytes and a loss of TREM2 are associated with an early stage of pathology in a mouse model of cerebral amyloid angiopathy.
cerebrovascular deposition of amyloid. The mechanisms underlying the contribution of CAA to neurodegeneration
Low-density lipoprotein receptor-related protein-1: a serial clearance homeostatic mechanism controlling Alzheimer's amyloid β-peptide elimination from the brain.
cerebrovascular and brain Aβ accumulation (hit 1) which then further amplifies neurovascular dysfunction (hit 2) preceding neurodegeneration
Modifications of physical and functional integrity of the blood-brain barrier in an inducible mouse model of neurodegeneration.
cerebrovascular volume and an increased basement membrane thickness may be more specifically associated with pTau in mouse models of neurodegeneration
Vascular Cognitive Impairment (VCI).
neurodegeneration including Alzheimer's disease (AD) and AD-related dementia. VCI accounts for at least 20-40% of all dementia diagnosis. Growing evidence indicates that cerebrovascular
Traumatic Brain Injury and Blood-Brain Barrier (BBB): Underlying Pathophysiological Mechanisms and the Influence of Cigarette Smoking as a Premorbid Condition.
neurodegeneration. Herein, we present a review highlighting the significant post-traumatic effects of TBI on the cerebrovascular
Neurodegeneration: 2024 update.
cerebrovascular pathologies over 25 years, associations between RHI and TDP-43 / hippocampal sclerosis, microglia / T-cell interaction in neurodegeneration
Biofluid biomarkers in Alzheimer's disease and other neurodegenerative dementias.
neurodegeneration, glial reactivity, α-synuclein pathology, TAR DNA-binding protein 43 (TDP-43) pathology, synaptic pathophysiology and cerebrovascular
Multi-analyte proteomic analysis identifies blood-based neuroinflammation, cerebrovascular and synaptic biomarkers in preclinical Alzheimer's disease.
cerebrovascular markers PGF, PDGFRB, and VEFGA; all previously linked to AD but only reliably measured in cerebrospinal fluid. SQSTM1, the autophagosome cargo protein, exhibited a significant association with neurodegeneration
Parkinson's Disease: From Pathogenesis to Pharmacogenomics.
neurodegeneration is likely to occur several decades before the onset of the motor symptoms. Potential risk factors include environmental toxins, drugs, pesticides, brain microtrauma, focal cerebrovascular
Multi-analyte proteomic analysis identifies blood-based neuroinflammation, cerebrovascular and synaptic biomarkers in preclinical Alzheimer's disease.
neurodegeneration (AT(N) statuses) were evaluated with [11C] PiB PET, [18F]AV-1451 PET, and an MRI-based AD-signature composite cortical thickness index, respectively. Linear mixed models were used
Blood-Brain Barrier Breakdown in Alzheimer's Disease: Mechanisms and Targeted Strategies.
neurodegeneration. The intricate relationship between the BBB and the pathogenesis of AD, especially in the context of neurovascular coupling and the overlap of pathophysiology in neurodegenerative and cerebrovascular
ApoA-I deficiency increases cortical amyloid deposition, cerebral amyloid angiopathy, cortical and hippocampal astrogliosis, and amyloid-associated astrocyte reactivity in APP/PS1 mice.
neurodegeneration and memory loss. The majority of AD patients also have Aβ deposition in cerebral vessels known as cerebral amyloid angiopathy (CAA), microhemorrhages, and vascular co-morbidities, suggesting that cerebrovascular
Single-photon emission tomography.
cerebrovascular reserve. After traumatic brain injury, SPECT has shown perfusion abnormalities despite normal morphology. In the context of organ donation, the diagnosis of brain death can be made with high
Apolipoprotein E and Alzheimer disease: pathobiology and targeting strategies.
neurodegeneration and microglial responses to AD-related pathologies. In addition, APOE4 is either pathogenic or shows reduced efficiency in multiple brain homeostatic pathways, including lipid transport, synaptic integrity and plasticity