Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis. - Wikidata - wikimedia - TriplyDB

Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis.

Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis.

http://www.wikidata.org/entity/Q37013605

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Toward more predictive genetic mouse models of Alzheimer's disease Targeting the proper amyloid-beta neuronal toxins: a path forward for Alzheimer's disease immunotherapeutics Three dimensions of the amyloid hypothesis: time, space and 'wingmen'Genetic modulation of soluble Aβ rescues cognitive and synaptic impairment in a mouse model of Alzheimer's disease Longitudinal testing of hippocampal plasticity reveals the onset and maintenance of endogenous human Aß-induced synaptic dysfunction in individual freely behaving pre-plaque transgenic rats: rapid reversal by anti-Aß agents.Caspase-2 is required for dendritic spine and behavioural alterations in J20 APP transgenic mice.Cannabinoid CB2 Receptors in a Mouse Model of Aβ Amyloidosis: Immunohistochemical Analysis and Suitability as a PET Biomarker of Neuroinflammation The keystone of Alzheimer pathogenesis might be sought in Aβ physiology Murine Aβ over-production produces diffuse and compact Alzheimer-type amyloid deposits.Normal cognition in transgenic BRI2-Aβ mice.Early detection of cryptic memory and glucose uptake deficits in pre-pathological APP mice Response to comments on "ApoE-directed therapeutics rapidly clear β-amyloid and reverse deficits in AD mouse models"Early enriched environment exposure protects spatial memory and accelerates amyloid plaque formation in APP(Swe)/PS1(L166P) mice.Amyloid β-protein oligomers and Alzheimer's disease.Imaging of cerebrovascular pathology in animal models of Alzheimer's disease Interpreting Alzheimer's disease clinical trials in light of the effects on amyloid-β.β-Amyloid peptides and amyloid plaques in Alzheimer's disease.Discrete pools of oligomeric amyloid-β track with spatial learning deficits in a mouse model of Alzheimer amyloidosis.Practical considerations for choosing a mouse model of Alzheimer's disease.Human Brain-Derived Aβ Oligomers Bind to Synapses and Disrupt Synaptic Activity in a Manner That Requires APP.Conditional Deletion of Prnp Rescues Behavioral and Synaptic Deficits after Disease Onset in Transgenic Alzheimer's Disease.

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Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis.

http://www.wikidata.org/entity/Q37013605

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on February 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Reversible pathologic and cogn ...... odel of Alzheimer-amyloidosis.

@en

Reversible pathologic and cogn ...... odel of Alzheimer-amyloidosis.

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type

label

Reversible pathologic and cogn ...... odel of Alzheimer-amyloidosis.

@en

Reversible pathologic and cogn ...... odel of Alzheimer-amyloidosis.

@nl

prefLabel

Reversible pathologic and cogn ...... odel of Alzheimer-amyloidosis.

@en

Reversible pathologic and cogn ...... odel of Alzheimer-amyloidosis.

@nl

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JNEUROSCI.4251-12.2013

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Journal of Neuroscience

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Reversible pathologic and cogn ...... odel of Alzheimer-amyloidosis.

@en

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Alena Savonenko

http://www.w3.org/2001/XMLSchema#string

Ashleigh Price

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Brenda D Moore

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David R Borchelt

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Deidre Lee

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Guilian Xu

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HyunSu Kim

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Kevin M Felsenstein

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Susan Fromholt

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Tatiana Melnikova

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P2860

Persistent amyloidosis following suppression of Abeta production in a transgenic model of Alzheimer disease

Correlative Memory Deficits, Abeta Elevation, and Amyloid Plaques in Transgenic Mice

Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain

Deciphering the genetic basis of Alzheimer's disease

Presenilin clinical mutations can affect gamma-secretase activity by different mechanisms

Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice

Secreted amyloid beta-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease

Memory impairment in transgenic Alzheimer mice requires cellular prion protein.

BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions.

Beta-secretase inhibitor GRL-8234 rescues age-related cognitive decline in APP transgenic mice.

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3765-3779

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scholarly article

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10.1523/JNEUROSCI.4251-12.2013

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2013-02-01T00:00:00Z

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23447589

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Alzheimer's disease

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3711622

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