Preservation of cell-survival mechanisms by the presenilin-1 K239N mutation may cause its milder clinical phenotype-Reference-Cited by-同舟云学术

Preservation of cell-survival mechanisms by the presenilin-1 K239N mutation may cause its milder clinical phenotype

Published:2016-10 Issue: Volume:46 Page:169-179
ISSN:0197-4580
Container-title:Neurobiology of Aging
language:en
Short-container-title:Neurobiology of Aging

Author:

Sarroca Sara,Molina-Martínez Patricia,Aresté Cristina,Etzrodt Martin,García de Frutos Pablo,Gasa Rosa,Antonell Anna,Molinuevo José Luís,Sánchez-Valle Raquel,Saura Carlos A.,Lladó Albert,Sanfeliu Coral

Funder

Ministerio de Economía y Competitividad

Instituto de Salud Carlos III

European Regional Development Fund

Publisher

Elsevier BV

Subject

Geriatrics and Gerontology,Developmental Biology,Neurology (clinical),Aging,General Neuroscience

Reference66 articles.

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3. Oxidative stress and lipid peroxidation are upstream of amyloid pathology;Arimon;Neurobiol. Dis.,2015

4. Wild-type but not FAD mutant presenilin-1 prevents neuronal degeneration by promoting phosphatidylinositol 3-kinase neuroprotective signaling;Baki;J. Neurosci.,2008

5. Presenilin clinical mutations can affect γ-secretase activity by different mechanisms;Bentahir;J. Neurochem.,2006

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