EZBRAIN42

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关键词:'EZBRAIN42'

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Efficient recovery of proteins from multiple source samples after TRIzol(®) or TRIzol(®)LS RNA extraction and long-term storage.

André E S Simões et al.

BMC genomics, 14, 181-181 (2013-03-19)

Simultaneous isolation of nucleic acids and proteins from a single biological sample facilitates meaningful data interpretation and reduces time, cost and sampling errors. This is particularly relevant for rare human and animal specimens, often scarce, and/or irreplaceable. TRIzol(®) and TRIzol(®)LS

Wnt signaling loss accelerates the appearance of neuropathological hallmarks of Alzheimer's disease in J20-APP transgenic and wild-type mice.

Cheril Tapia-Rojas et al.

Journal of neurochemistry, 144(4), 443-465 (2017-12-15)

Alzheimer's disease (AD) is a neurodegenerative pathology characterized by aggregates of amyloid-β (Aβ) and phosphorylated tau protein, synaptic dysfunction, and spatial memory impairment. The Wnt signaling pathway has several key functions in the adult brain and has been associated with

Sustained Alzheimer's amyloid pathology in myeloid differentiation protein-88-deficient APPswe/PS1 mice.

Y Goll et al.

Neuro-degenerative diseases, 13(2-3), 58-60 (2013-11-07)

Most Alzheimer's disease (AD) cases arise sporadically and may involve innate immune activation of microglial expressed Toll-like receptors regulated through the myeloid differentiation protein 88 (MyD88) pathway. It was the aim of this study to test the innate immune involvement

Hippocampal proNGF signaling pathways and β-amyloid levels in mild cognitive impairment and Alzheimer disease.

Elliott J Mufson et al.

Journal of neuropathology and experimental neurology, 71(11), 1018-1029 (2012-10-26)

Hippocampal precursor of nerve growth factor (proNGF)/NGF signaling occurs in conjunction with β-amyloid (Aβ) accumulations in Alzheimer disease (AD). To assess the involvement of this pathway in AD progression, we quantified these proteins and their downstream pathway activators in postmortem

Chronic GluN2B antagonism disrupts behavior in wild-type mice without protecting against synapse loss or memory impairment in Alzheimer's disease mouse models.

Jesse E Hanson et al.

The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(24), 8277-8288 (2014-06-13)

Extensive evidence implicates GluN2B-containing NMDA receptors (GluN2B-NMDARs) in excitotoxic-insult-induced neurodegeneration and amyloid β (Aβ)-induced synaptic dysfunction. Therefore, inhibiting GluN2B-NMDARs would appear to be a potential therapeutic strategy to provide neuroprotection and improve cognitive function in Alzheimer's disease (AD). However, there

Is L-methionine a trigger factor for Alzheimer's-like neurodegeneration?: Changes in Aβ oligomers, tau phosphorylation, synaptic proteins, Wnt signaling and behavioral impairment in wild-type mice.

Cheril Tapia-Rojas et al.

Molecular neurodegeneration, 10, 62-62 (2015-11-23)

L-methionine, the principal sulfur-containing amino acid in proteins, plays critical roles in cell physiology as an antioxidant and in the breakdown of fats and heavy metals. Previous studies suggesting the use of L-methionine as a treatment for depression and other

Dysregulation of 14-3-3 proteins in neurodegenerative diseases with Lewy body or Alzheimer pathology.

Michael B McFerrin et al.

Annals of clinical and translational neurology, 4(7), 466-477 (2017-07-12)

The highly conserved 14-3-3 proteins interact with key players involved in Parkinson's disease (PD) and other neurodegenerative disorders. We recently demonstrated that 14-3-3 phosphorylation is increased in PD models and that increased 14-3-3 phosphorylation reduces the neuroprotective effects of 14-3-3

Tetrahydrohyperforin Inhibits the Proteolytic Processing of Amyloid Precursor Protein and Enhances Its Degradation by Atg5-Dependent Autophagy.

Viviana A Cavieres et al.

PloS one, 10(8), e0136313-e0136313 (2015-08-27)

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid-β (Aβ) peptide. We have previously shown that the compound tetrahydrohyperforin (IDN5706) prevents accumulation of Aβ species in an in vivo model of AD, however the mechanism that

Inhibition of Wnt signaling induces amyloidogenic processing of amyloid precursor protein and the production and aggregation of Amyloid-β (Aβ)42 peptides.

Cheril Tapia-Rojas et al.

Journal of neurochemistry, 139(6), 1175-1191 (2016-10-26)

Alzheimer's disease (AD) is the most common neurodegenerative disorder and the most frequent cause of dementia in the aged population. According to the amyloid hypothesis, the amyloid-β (Aβ) peptide plays a key role in the pathogenesis of AD. Aβ is

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