PS-1 expressed weakly in three medication groups along with augmentation of dosage.
2
However a higher frequency of PS-1 heterozygotes in the demented DS group was noted.
3
The levels of Abeta were found to correlate statistically with the expression of PS-1.
4
Allele frequencies at PS-1 and ACT polymorphisms in people with DS were compared to those in age-matched controls.
5
However, we found an unexpected differential effect of PS-1 but not APP717 mutation cases.
6
There were no frequency differences between the control sample and DS sample for PS-1 or ACT alleles or genotypes.
7
Results: The expression of PS-1 in rat hippocampus of senile control group was stronger than that of adult control group.
8
These findings suggest that the induction of PS-1 genes may be associated with some responses of neurons damaged by transient ischemia.
9
We conclude that unlike the general population, neither PS-1 nor ACT polymorphisms appear to have a similar detrimental effect on dementia in DS.
10
Thus, we have been unable to find an association between the PS-1 intronic polymorphism and early- or late-onset AD within this autopsy-confirmed population.
11
Thus, APP and PS-1 mutations predominantly affect the CA regions with profound neurodegeneration, which contributes early and severe clinical features of familial AD.
12
These results suggest that the PS-1 polymorphism, or a locus in linkage disequilibrium with it, acts as a risk factor for late onset AD.
13
Result: PCR-SSCP showed abnormality in PS-1 exon 5 among 5 AD patients and 4 AD family members without AD symptoms.
14
From 1 day to 3 day-reperfusion after 5 min-ischemia, PS-1 mRNA was induced in the hippocampus compared with the sham-operated control.
15
The cells which induced the PS-1 genes were neurons of CA3 and dentate gyrus, the region relatively resistant to ischemic stress.
16
Immobilization of a potent GSM onto an agarose matrix quantitatively recovered Pen-2 and to a lesser degree PS-1 NTFs from cellular extracts.