Letters to the EditorMisserise mutation of S182 gene in Italian families with early-onset Alzheimer's disease
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Cited by (65)
Hippocampal proteomics defines pathways associated with memory decline and resilience in normal aging and Alzheimer's disease mouse models
2017, Behavioural Brain ResearchCitation Excerpt :The extent to which these previously reported behavioral and neuronal changes observed in 5XFAD and Ntg mice correspond to dysfunction of the same molecular pathways is currently unknown. To identify altered proteins and pathways associated with the development of normal aging and AD memory deficits, this study exploited individual differences in the memory abilities of 8-month-old B6SJL mice harboring human mutations in the genes for amyloid precursor protein (APP) and presenilin1 (PSEN1), which are known to cause early-onset familial AD (5XFAD model), and their Ntg littermates [12–16]. Mice were diagnosed as having either intact or impaired memory based on their CFM performance relative to a previously tested group of 2-month-old controls [9,11], and LC–MS/MS was used to quantify hippocampal membrane proteins across groups.
Structure nor stability of the transmembrane spanning 6/7 domain of presenilin I correlates with pathogenicity
2007, Biochemical and Biophysical Research CommunicationsClinical, Pathological, and Biochemical Spectrum of Alzheimer Disease Associated with PS-1 Mutations
2004, American Journal of Geriatric PsychiatryActivated cAMP-response Element-binding Protein Regulates Neuronal Expression of Presenilin-1
2001, Journal of Biological ChemistryImplication of α1-antichymotrypsin polymorphism in familial Alzheimer's disease
1998, Neuroscience Letters