Physician
Neurology
Karen H. Ashe
|
|
Give Review
Karen H. Ashe works in the field of Neurology. She went to medical school at Harvard Medical School. Harvard Medical School is a top medical college. Harvard Medical School is ranked 1 in research and 12 in primary care medicine She has 1 awards "Elected Member". Karen Ashe is a published doctor. She has 53 papers published. The most current publication "More than a FAD: The InVivo Effects of Disease-Linked Presenilin-1 Mutations."
Publications
- More than a FAD: The In Vivo Effects of Disease-Linked Presenilin-1 Mutations.
- Correlation of specific amyloid-β oligomers with tau in cerebrospinal fluid from cognitively normal older adults.
- Brain amyloid-? oligomers in ageing and Alzheimer's disease.
- Prions, prionoids and pathogenic proteins in Alzheimer disease.
- Propagation of tau pathology in a model of early Alzheimer''s disease.
- Neurobiology of disease.
- Cognitive effects of cell-derived and synthetically derived A? oligomers.
- Grape seed polyphenolic extract specifically decreases aβ*56 in the brains of Tg2576 mice.
- Extended results of the Alzheimer''s disease anti-inflammatory prevention trial.
- Tau mislocalization to dendritic spines mediates synaptic dysfunction independently of neurodegeneration.
- Effect size of reference memory deficits in the Morris water maze in Tg2576 mice.
- ''Too much good news'' - are Alzheimer mouse models trying to tell us how to prevent, not cure, Alzheimer''s disease?
- Probing the biology of Alzheimer''s disease in mice.
- Oligomers of the amyloid-beta protein disrupt working memory: confirmation with two behavioral procedures.
- Amyloid-beta deposits lead to retinal degeneration in a mouse model of Alzheimer disease.
- Amyloid plaque and neurofibrillary tangle pathology in a regulatable mouse model of Alzheimer''s disease.
- Genes contributing to prion pathogenesis.
- Cyclooxygenase-2 inhibition improves amyloid-beta-mediated suppression of memory and synaptic plasticity.
- Plaque-bearing mice with reduced levels of oligomeric amyloid-beta assemblies have intact memory function.
- In vivo imaging reveals dissociation between caspase activation and acute neuronal death in tangle-bearing neurons.
- A tale about tau.
- Accelerating amyloid-beta fibrillization reduces oligomer levels and functional deficits in Alzheimer disease mouse models.
- Involvement of beta-site APP cleaving enzyme 1 (BACE1) in amyloid precursor protein-mediated enhancement of memory and activity-dependent synaptic plasticity.
- Accumulation of pathological tau species and memory loss in a conditional model of tauopathy.
- In search of the molecular basis of memory loss in Alzheimer disease.
- Molecular basis of memory loss in the Tg2576 mouse model of Alzheimer''s disease.
- Region-specific dissociation of neuronal loss and neurofibrillary pathology in a mouse model of tauopathy.
- A specific amyloid-beta protein assembly in the brain impairs memory.
- Age-dependent neurofibrillary tangle formation, neuron loss, and memory impairment in a mouse model of human tauopathy (P301L).
- The role of cell-derived oligomers of Abeta in Alzheimer''s disease and avenues for therapeutic intervention.
- Mechanisms of memory loss in Abeta and tau mouse models.
- Tau suppression in a neurodegenerative mouse model improves memory function.
- Natural oligomers of the amyloid-beta protein specifically disrupt cognitive function.
- Identification of loci determining susceptibility to the lethal effects of amyloid precursor protein transgene overexpression.
- Docosahexaenoic acid protects from dendritic pathology in an Alzheimer''s disease mouse model.
- Dimeric amyloid beta protein rapidly accumulates in lipid rafts followed by apolipoprotein E and phosphorylated tau accumulation in the Tg2576 mouse model of Alzheimer...
- Motor dysfunction and gliosis with preserved dopaminergic markers in human alpha-synuclein A30P transgenic mice.
- Altered short-term hippocampal synaptic plasticity in mutant alpha-synuclein transgenic mice.
- Neurotoxic effects of thioflavin S-positive amyloid deposits in transgenic mice and Alzheimer's disease.
- Reversible memory loss in a mouse transgenic model of Alzheimer's disease.
- The relationship between Abeta and memory in the Tg2576 mouse model of Alzheimer's disease.
- Learning and memory in transgenic mice modeling Alzheimer''s disease.
- Beta-amyloid activates the mitogen-activated protein kinase cascade via hippocampal alpha7 nicotinic acetylcholine receptors: In vitro and in vivo mechanisms related t...
- Synaptic structure and function in transgenic APP mice.
- Age-dependent changes in brain, CSF, and plasma amyloid (beta) protein in the Tg2576 transgenic mouse model of Alzheimer's disease.
- Abeta 1-40-related reduction in functional hyperemia in mouse neocortex during somatosensory activation.
- Ibuprofen suppresses plaque pathology and inflammation in a mouse model for Alzheimer''s disease.
- Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model.
- Plaque-associated alpha-synuclein (NACP) pathology in aged transgenic mice expressing amyloid precursor protein.
- Evidence for glial-mediated inflammation in aged APP(SW) transgenic mice.
- Serum amyloid P is not present in amyloid beta deposits of a transgenic animal model.
- β-Amyloid oligomers in aging and Alzheimer's disease.
Doctors Specialties
- Neurology
Accepted Insurances
Awards
- Elected Member
Education
-
Harvard Medical School
Helpful Reviews
Similar Doctors
|
|
Dr. Vivian K. Fink, MD
 This Doctor is OpenDoctor Recommended.
|
|
|
Dr. Steven F. Noran, MD
This Doctor is OpenDoctor Recommended.
|
|
|
Dr. Richard F. Shronts, MD
This Doctor is OpenDoctor Recommended.
|
|
|
Dr. Milton G. Ettinger, MD |
|
|
Dr. Elizabeth Haule, MD |
|
|
Dr. Jae H. Kim, MD |
|
|
Dr. Pezhman Roohani, MD
This Doctor is OpenDoctor Recommended.
|