ADAM30 Downregulates APP-Linked Defects Through Cathepsin D Activation in Alzheimer's Disease.
Letronne F, Laumet G, Ayral AM, Chapuis J, Demiautte F, Laga M, Vandenberghe ME, Malmanche N, Leroux F, Eysert F, Sottejeau Y, Chami L, Flaig A, Bauer C, Dourlen P, Lesaffre M, Delay C, Huot L, Dumont J, Werkmeister E, Lafont F, Mendes T, Hansmannel F, Dermaut B, Deprez B, Hérard AS, Dhenain M, Souedet N, Pasquier F, Tulasne D, Berr C, Hauw JJ, Lemoine Y, Amouyel P, Mann D, Déprez R, Checler F, Hot D, Delzescaux T, Gevaert K, Lambert JC.
Letronne F, et al. Among authors: pasquier f.
EBioMedicine. 2016 Jul;9:278-292. doi: 10.1016/j.ebiom.2016.06.002. Epub 2016 Jun 2.
EBioMedicine. 2016.
PMID: 27333034
Free PMC article.
Accordingly, in Alzheimer-like transgenic mice, neuronal ADAM30 over-expression lowered Abeta42 secretion in neuron primary cultures, soluble Abeta42 and amyloid plaque load levels in the brain and concomitantly enhanced CTSD activity and finally rescued long term potentia …
Accordingly, in Alzheimer-like transgenic mice, neuronal ADAM30 over-expression lowered Abeta42 secretion in neuron primary cultures, solubl …