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Figure 2 | Alzheimer's Research & Therapy

Figure 2

From: Molecular consequences of amyloid precursor protein and presenilin mutations causing autosomal-dominant Alzheimer's disease

Figure 2

Tissue culture models of presenilin (PSEN) mutations. In most studies, PSEN mutants have been stably overexpressed either in permanent cells lines (left) or in PSEN1/PSEN2-/- double-knockout cell lines (middle). Due to the replacement phenomenon or the lack of endogenous wild type (WT) PSEN proteins, functional γ-secretase complexes in both of these tissue culture models contain predominantly or solely the exogenously expressed PSEN mutants. This situation is different from familial Alzheimer's disease (FAD) patients with heterozygous PSEN1 (or PSEN2) mutations that express mutant and WT PSEN1 (or PSEN2) in an equal ratio in the background of two WT PSEN2 (or PSEN1) alleles (right). CMV, cytomegalovirus.

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Alzheimer's Research & Therapy

ISSN: 1758-9193