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Pathological mechanism
Name
p35/Cdk5 pathway mediates soluble amyloid-beta peptide-induced tau phosphorylation in vitro
Description
Hypothesis
Dendritic Hypothesis - Ca++ currents
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Extracelular pathological element
Beta-amyloid (1-42)
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Intracelular pathological element
Tau protein
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Pathological action
Increases
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Process
Tau hyperphosphorylation
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Process action
Activates
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Transmitter(s)
Receptor(s)
Channel(s)
I L high threshold
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Pharmacological Agent
P35 Antisense Oligonucleotides
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Calpain Inhibitor I
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Verapamil
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Pharmacological Action
Blocks
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Brain region
Neuron
Cell model
Cellular compartment
PubMed ID
12125077
Citation
12125077
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AlzWeb
Notes
"p35/Cdk5 pathway mediates soluble amyloid-beta peptide-induced tau phosphorylation in vitro. ... Results show that sAbeta(1-42) at relatively low levels (1-5 microM) dose-dependently increases tau phosphorylation at AD-specific phosphoepitopes in differentiated N2a/p35 cells compared with controls, an effect that is blocked by antisense oligonucleotides against p35. sAbeta(1-42)-induced tau phosphorylation is concomitant with an increase in both p25 to p35 ratio and Cdk5 activity (but not protein levels). Additionally, blockade of L-type calcium channels or inhibition of calpain completely abolishes this effect." (Town et al. 2002)
Pathology
Alzheimer
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Stage
Question
Claim
Aß causes increased Ca++ influx by activation of L-type Ca++ channels
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Other categories referring to "
p35/Cdk5 pathway mediates soluble amyloid-beta peptide-induced tau phosphorylation in vitro
"
Revisions:
12
Last time:
11/21/2008 12:23:20 PM
Reviewer:
Pradeep Mutalik
Owner:
Tom Morse
This database was supported by the Human Brain Project (NIDCD, NIMH, NIA, NICD, NINDS) and MURI (Multidisciplinary University Research Initiative). It is now supported by RO1 DC 009977 from the National Institute for Deafness and other Communication Disorders.
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