Neuron loss in the 5XFAD mouse model of Alzheimer's disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation. - Wikidata - awgldk - TriplyDB

Neuron loss in the 5XFAD mouse model of Alzheimer's disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation.

Neuron loss in the 5XFAD mouse model of Alzheimer's disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation.

http://www.wikidata.org/entity/Q36556213

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The low-density lipoprotein receptor-related protein 1 and amyloid-β clearance in Alzheimer's disease MT5-MMP is a new pro-amyloidogenic proteinase that promotes amyloid pathology and cognitive decline in a transgenic mouse model of Alzheimer's disease.Complex regulation of γ-secretase: from obligatory to modulatory subunits Analyzing dendritic spine pathology in Alzheimer's disease: problems and opportunities In vivo imaging of microglial activation by positron emission tomography with [(11)C]PBR28 in the 5XFAD model of Alzheimer's disease Synaptic deficits in layer 5 neurons precede overt structural decay in 5xFAD mice.Alzheimer amyloid beta inhibition of Eg5/kinesin 5 reduces neurotrophin and/or transmitter receptor function.Progranulin protects against amyloid β deposition and toxicity in Alzheimer's disease mouse models.Altered theta oscillations and aberrant cortical excitatory activity in the 5XFAD model of Alzheimer's disease.Eliminating microglia in Alzheimer's mice prevents neuronal loss without modulating amyloid-β pathology.Neuronal p38α mediates synaptic and cognitive dysfunction in an Alzheimer's mouse model by controlling β-amyloid production.1950 MHz Electromagnetic Fields Ameliorate Aβ Pathology in Alzheimer's Disease Mice Increased mtDNA mutations with aging promotes amyloid accumulation and brain atrophy in the APP/Ld transgenic mouse model of Alzheimer's disease.Voluntary Exercise Promotes Glymphatic Clearance of Amyloid Beta and Reduces the Activation of Astrocytes and Microglia in Aged Mice.Genetic inhibition of phosphorylation of the translation initiation factor eIF2α does not block Aβ-dependent elevation of BACE1 and APP levels or reduce amyloid pathology in a mouse model of Alzheimer's disease.Early detection of cerebral glucose uptake changes in the 5XFAD mouse.Development of a novel cellular model of Alzheimer's disease utilizing neurosphere cultures derived from B6C3-Tg(APPswe,PSEN1dE9)85Dbo/J embryonic mouse brain Molecular Differences and Similarities Between Alzheimer's Disease and the 5XFAD Transgenic Mouse Model of Amyloidosis.Abnormal vibrissa-related behavior and loss of barrel field inhibitory neurons in 5xFAD transgenics.Aβ-dependent reduction of NCAM2-mediated synaptic adhesion contributes to synapse loss in Alzheimer's disease.Temporal gene profiling of the 5XFAD transgenic mouse model highlights the importance of microglial activation in Alzheimer's disease.The γ-secretase complex: from structure to function.Increased fragmentation of sleep-wake cycles in the 5XFAD mouse model of Alzheimer's disease Transcriptional regulation of N-acetylaspartate metabolism in the 5xFAD model of Alzheimer's disease: evidence for neuron-glia communication during energetic crisis.Noradrenergic dysfunction in Alzheimer's disease.TREM2 lipid sensing sustains the microglial response in an Alzheimer's disease model.Transient Cerebral Ischemia Promotes Brain Mitochondrial Dysfunction and Exacerbates Cognitive Impairments in Young 5xFAD Mice.Synaptosomal Mitochondrial Dysfunction in 5xFAD Mouse Model of Alzheimer's Disease.Neurological dysfunctions associated with altered BACE1-dependent Neuregulin-1 signaling.Increased tauopathy drives microglia-mediated clearance of beta-amyloid.Neuronally-directed effects of RXR activation in a mouse model of Alzheimer's disease.The Role of PGRN in Alzheimer's Disease.EFAD transgenic mice as a human APOE relevant preclinical model of Alzheimer's disease.Inflammation in Alzheimer's disease: Lessons learned from microglia-depletion models.Limited Effects of Prolonged Environmental Enrichment on the Pathology of 5XFAD Mice.IRE1 signaling exacerbates Alzheimer's disease pathogenesis.Nanoplasmonic fiber tip probe detects significant reduction of intracellular Alzheimer's disease-related oligomers by curcumin.Naoling decoction restores cognitive function by inhibiting the neuroinflammatory network in a rat model of Alzheimer's disease.Chronic Progressive Neurodegeneration in a Transgenic Mouse Model of Prion Disease.Vulnerability of primary neurons derived from Tg2576 Alzheimer mice to oxygen and glucose deprivation: role of intraneuronal amyloid-β accumulation and astrocytes.

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Neuron loss in the 5XFAD mouse model of Alzheimer's disease correlates with intraneuronal Aβ42 accumulation and Caspase-3 activation.

http://www.wikidata.org/entity/Q36556213

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2013 nî lūn-bûn

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name

Neuron loss in the 5XFAD mouse ...... tion and Caspase-3 activation.

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Neuron loss in the 5XFAD mouse ...... tion and Caspase-3 activation.

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Neuron loss in the 5XFAD mouse ...... tion and Caspase-3 activation.

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Neuron loss in the 5XFAD mouse ...... tion and Caspase-3 activation.

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Neuron loss in the 5XFAD mouse ...... tion and Caspase-3 activation.

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Neuron loss in the 5XFAD mouse ...... tion and Caspase-3 activation.

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Molecular Neurodegeneration

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Neuron loss in the 5XFAD mouse ...... tion and Caspase-3 activation.

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Robert Vassar

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William A Eimer

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P2860

Hippocampal neuron loss exceeds amyloid plaque load in a transgenic mouse model of Alzheimer's disease

A pathogenic mutation for probable Alzheimer's disease in the APP gene at the N-terminus of beta-amyloid

Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease

Intracellular amyloid-beta in Alzheimer's disease

Massive CA1/2 neuronal loss with intraneuronal and N-terminal truncated Abeta42 accumulation in a novel Alzheimer transgenic model

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

Mechanism of amyloid plaque formation suggests an intracellular basis of Abeta pathogenicity.

Identification of low molecular weight pyroglutamate A{beta} oligomers in Alzheimer disease: a novel tool for therapy and diagnosis

Alzheimer's disease: perspectives for the new millennium

BACE1 (beta-secretase) knockout mice do not acquire compensatory gene expression changes or develop neural lesions over time.

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Alzheimer's disease

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