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P4–424: β–synuclein derived small peptides for treatment of Alzheimer's disease
Author(s) -
Windisch Manfred,
Wronski Robert,
Prokesch Manuela,
Hutter-Paier Birgit
Publication year - 2006
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2006.05.2166
Subject(s) - neurodegeneration , alpha synuclein , neuroprotection , oxidative stress , synuclein , in vivo , synucleinopathies , amyloid (mycology) , protein aggregation , biology , microbiology and biotechnology , amyloid beta , peptide sequence , neuroscience , parkinson's disease , peptide , biochemistry , disease , medicine , gene , genetics , botany
variants ( 30, 43, 47 & 60 kDa) were detected by immunoblot analysis, and like pituitary gonadotropes, their expression was upregulated by low and downregulated by high, GnRH concentrations. Conclusions: These results indicate that GnRH can signal via neuronal GnRH receptors to modulate G-protein coupling and LH expression, and explains the elevation in LH expression in pyramidal neurons of AD compared with agematched control brain. Suppression of menopause-induced elevations in neuronal GnRH receptor signaling with leuprolide might explain the efficacy of this drug in stabilizing cognition in AD.