Methods. Standardized magnetic resonance imaging was performed on 1,403 women, 1-4 years after they had participated in randomized placebo-controlled clinical trials of CEE-based therapies. Women included in this report were aged 65-80 years and free of dementia and mild cognitive impairment (MCI) when originally enrolled in the trials, which lasted an average find more of 4-6 years and were conducted at 14 academic U. S. medical centers. The associations that regional brain volumes and ischemic lesion volumes had with the development of cognitive impairment (i.e., dementia or MCI) were contrasted

between treatment groups using analyses of covariance.

Results. Fifty-three women developed MCI or probable dementia during follow-up. Among women who had been prescribed CEE-based therapies, cognitive impairment was associated with relatively smaller hippocampal (p =.0002) and total brain volumes (p =.03). Qualitatively, these associations appeared to be independent of their level of pretreatment cognitive function. Among women who had been prescribed

placebo, these relationships were not evident; instead, cognitive impairment was associated with greater ischemic lesion volume in the frontal lobe (p =.007) and overall (p =.02).

Conclusion. A mechanism by which CEE-based postmenopausal hormone therapy induces cognitive impairment appears to be through increased brain atrophy.”
“Recent evidences indicate that SC75741 nmr polymorphisms within the promoter region of the vascular endothelial growth factor (VEGF) gene may elevate the risk for Alzheimer’s disease (AD). To further investigate, we have analyzed association between promoter polymorphisms of the VEGF gene in 93 AD patients and age and sex

matched 113 controls from Tunisian population. The distribution of genotype and allele frequencies of the VEGF (-2578C/A) and (-1154G/A) polymorphisms did not differ H 89 in vivo significantly between AD and control groups (p > 0.05). In the subgroup of ApoE epsilon 4 carriers, the -2578A was observed to be significantly higher in the AD patients than in the control individuals. After adjusting the data by gender, age and the ApoE e4 status using logistic regression, the -2578A allele was found to increase the risk for sporadic AD by 1.7-fold. The present study provides the evidence that the -2578A allele may be associated with the development of AD in the individuals with ApoE epsilon 4 allele. In addition, AD patients carrying the -2578A allele had lower A beta 42 (p = 0.029) levels than those without this allele, particularly in subjects with ApoE epsilon 4 allele. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Background. Few cohort studies have adequate numbers of carefully reviewed deaths to allow an analysis of unique and shared risk factors for cause-specific mortality.