Transgenic mice overexpressing APP and transforming growth factor-beta1 feature cognitive and vascular hallmarks of Alzheimer's disease - Wikidata - wikimedia - TriplyDB

Transgenic mice overexpressing APP and transforming growth factor-beta1 feature cognitive and vascular hallmarks of Alzheimer's disease

Transgenic mice overexpressing APP and transforming growth factor-beta1 feature cognitive and vascular hallmarks of Alzheimer's disease

http://www.wikidata.org/entity/Q34358146

about

The neuroprotective functions of transforming growth factor beta proteins Pioglitazone improves reversal learning and exerts mixed cerebrovascular effects in a mouse model of Alzheimer's disease with combined amyloid-β and cerebrovascular pathology Neurovascular pathways to neurodegeneration in Alzheimer's disease and other disorders Neurovascular abnormalities in brain disorders: highlights with angiogenesis and magnetic resonance imaging studies.Effects of hypoperfusion in Alzheimer's disease.Neuroanatomical correlates of atrial fibrillation: a longitudinal MRI study.Neurovascular function in Alzheimer's disease patients and experimental models.Sex differences in TGFB-β signaling with respect to age of onset and cognitive functioning in schizophrenia.Neurovascular dysfunction and faulty amyloid β-peptide clearance in Alzheimer disease.Vascular cognitive impairment: Modeling a critical neurologic disease in vitro and in vivo.Endothelial TRPV4 channels mediate dilation of cerebral arteries: impairment and recovery in cerebrovascular pathologies related to Alzheimer's disease The potential role of proinflammatory and antiinflammatory cytokines in Alzheimer disease pathogenesis.Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer's disease.Alpha-Smooth Muscle Actin mRNA and Protein Are Increased in Isolated Brain Vessel Extracts of Alzheimer Mice.Losartan improves cerebrovascular function in a mouse model of Alzheimer's disease with combined overproduction of amyloid-β and transforming growth factor-β1.NMR-Based Metabolic Profiling Reveals Neurochemical Alterations in the Brain of Rats Treated with Sorafenib.Enhanced expressions of neurodegeneration-associated factors, UPS impairment, and excess Aβ accumulation in the hippocampus of mice with persistent cerebral toxocariasis.Enalapril Alone or Co-Administered with Losartan Rescues Cerebrovascular Dysfunction, but not Mnemonic Deficits or Amyloidosis in a Mouse Model of Alzheimer's Disease.

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P2860

Transgenic mice overexpressing APP and transforming growth factor-beta1 feature cognitive and vascular hallmarks of Alzheimer's disease

http://www.wikidata.org/entity/Q34358146

description

2010 nî lūn-bûn

@nan

2010 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

@zh-hant

2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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type

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

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AJPATH.2010.100339

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The American Journal of Pathology

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Transgenic mice overexpressing ...... llmarks of Alzheimer's disease

@en

P2093

Brice Ongali

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Clotilde Lecrux

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Edith Hamel

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Nektaria Nicolakakis

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Panayiota Papadopoulos

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Tahar Aboulkassim

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Xin-Kang Tong

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P2860

beta-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease

High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation

Neurovascular regulation in the normal brain and in Alzheimer's disease

Nox2-derived radicals contribute to neurovascular and behavioral dysfunction in mice overexpressing the amyloid precursor protein.

Intact memory in TGF-β1 transgenic mice featuring chronic cerebrovascular deficit: recovery with pioglitazone

Is Alzheimer's disease a neurodegenerative or a vascular disorder? Data, dogma, and dialectics.

NADPH-oxidase-derived reactive oxygen species mediate the cerebrovascular dysfunction induced by the amyloid beta peptide.

Collagen VI protects neurons against Abeta toxicity.

Alzheimer's disease and vascular dementia in developing countries: prevalence, management, and risk factors.

Categorical and correlational analyses of baseline fluorodeoxyglucose positron emission tomography images from the Alzheimer's Disease Neuroimaging Initiative (ADNI).

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3071-3080

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scholarly article

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10.2353/AJPATH.2010.100339

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6

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177

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Pedro Rosa-Neto

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2010-11-18T00:00:00Z

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47815368

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21088218

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Alzheimer's disease

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2993264

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