Elsevier

The Lancet

Volume 346, Issue 8972, 12 August 1995, Pages 439-440
The Lancet

Letters to the Editor
Misserise mutation of S182 gene in Italian families with early-onset Alzheimer's disease

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    Protective effect of apolipoprotein E type 2 allele decreases risk of late onset Alzheimer's disease

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    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.

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