(Q28376637)

2

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Y Qian

3

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W Wei

4

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R Chen

5

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D Chuang

European Journal of Pharmacology

6

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language of work or name

English

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publication date

31 March 2000

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published in

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volume

392

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page(s)

117-23

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issue

3

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cites work

Lithium protects cultured neurons against beta-amyloid-induced neurodegeneration.

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Vitamin E protects nerve cells from amyloid beta protein toxicity

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BCL-2 prevents killing of neuronal cells by glutamate but not by amyloid beta protein

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Lithium activates the serine/threonine kinase Akt-1 and suppresses glutamate-induced inhibition of Akt-1 activity in neurons

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Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity

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Role of potassium channels in amyloid-induced cell death.

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Secreted forms of beta-amyloid precursor protein protect hippocampal neurons against amyloid beta-peptide-induced oxidative injury.

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Tyrosine kinase inhibitors and cycloheximide inhibit Li+ protection of cerebellar granule neurons switched to non-depolarizing medium.

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Lithium reduces tau phosphorylation by inhibition of glycogen synthase kinase-3.

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Beta-amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage

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beta-Amyloid precursor protein metabolites and loss of neuronal Ca2+ homeostasis in Alzheimer's disease.

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Lithium inhibits Alzheimer's disease-like tau protein phosphorylation in neurons.

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Neuroprotective effects of chronic lithium on focal cerebral ischemia in rats

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Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx

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Amyloid beta peptide of Alzheimer's disease downregulates Bcl-2 and upregulates bax expression in human neurons

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Alzheimer's disease: genetic studies and transgenic models

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The molecular pathology of Alzheimer's disease

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Inhibition of PC12 cell redox activity is a specific, early indicator of the mechanism of beta-amyloid-mediated cell death

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The use of psychotropic medication in the management of problem behaviors in the patient with Alzheimer's disease.

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Genetic heterogeneity of gene defects responsible for familial Alzheimer disease

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Inhibition of amyloid beta protein aggregation and neurotoxicity by rifampicin. Its possible function as a hydroxyl radical scavenger.

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Evidence that glyceraldehyde-3-phosphate dehydrogenase is involved in age-induced apoptosis in mature cerebellar neurons in culture.

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inferred from DOI database lookup

7 January 2021

based on heuristic

Identifiers

DOI

10.1016/S0014-2999(00)00127-8

0 references

Fatcat ID

release_jowj3dcjsjerpmc75orpjwkdwi

1 reference

Fatcat

https://api.fatcat.wiki/v0/release/jowj3dcjsjerpmc75orpjwkdwi