Zimmermann_2005_Neurobiol.Dis_19_237

Reference

Title : Cholinesterase inhibitors influence APP metabolism in Alzheimer disease patients - Zimmermann_2005_Neurobiol.Dis_19_237
Author(s) : Zimmermann M , Borroni B , Cattabeni F , Padovani A , Di Luca M
Ref : Neurobiol Dis , 19 :237 , 2005
Abstract :

Platelets mirror pathogenic alterations in the central nervous system of Alzheimer disease (AD) patients: an alteration of the Amyloid Precursor Protein (APP) forms pattern and decreased alpha-secretase activity--the non-amyloidogenic APP processing enzyme--were demonstrated. Platelets were analysed at baseline and after 30 days of cholinesterase inhibitor (ChEI) treatment (T30). ADAM10 levels, alpha- and beta-secretase activity were assessed measuring ADAM10 immunoreactivity, sAPPalpha release and the membrane-attached C-terminal fragments produced by beta- and alpha-secretase cleavage, that is, CTF99 and CTF83, respectively. ChEIs treatment rescues impaired APP metabolism increasing significantly ADAM10 levels (T30 vs. T0, P < 0.05), alpha-secretase activity (T30 vs. T0, P < 0.05) and reducing beta-secretase cleavage (T30 vs. T0, P < 0.05). Restoration of the balance between the mutually exclusive alpha- and beta-secretase pathway in APP processing caused by short-term ChEIs treatment potentially represents a key event in AD therapy linking in vivo cholinergic effect to APP metabolism. The use of platelets may represent a useful tool to follow molecular aspects of pharmacological response in AD patients.

PubMedSearch : Zimmermann_2005_Neurobiol.Dis_19_237
PubMedID: 15837579

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Citations formats

Zimmermann M, Borroni B, Cattabeni F, Padovani A, Di Luca M (2005)
Cholinesterase inhibitors influence APP metabolism in Alzheimer disease patients
Neurobiol Dis 19 :237

Zimmermann M, Borroni B, Cattabeni F, Padovani A, Di Luca M (2005)
Neurobiol Dis 19 :237