57 mg/100 mg of fatty acid below normal verses 0.59 mg/100 mg for docosahexaenoic acid. Plasma/serum arachidonic acid was even lower; GW786034 cost 0.71 mg/100 mg of fatty acid below normal verses 0.34 mg/100 mg for docosahexaenoic acid. The origin, consequences and relative importance of subnormal arachidonic acid to brain function bears further investigation. (C) 2009 Elsevier Ltd. All rights reserved.”
“Objectives. To estimate the causal effect of coresidence with an adult child on depressive symptoms

among older widowed women in South Korea.

Method. Data from the first (2006) and second (2008) waves of the Korea Longitudinal Study of Ageing were used. The analysis was restricted to widowed women aged >= 65 years with at least one living child (N = 2,446). We used an instrumental variables (IVs) estimation exploiting two child characteristics as IVs (the number of sons and whether the eldest child is a daughter). Specification tests for IVs showed that these instruments predict the probability of an older widowed woman’s coresidence with an adult child but do not directly affect depressive symptoms.

Results. Our IV two-stage least-squares estimator suggested that coresidence with an adult child has a protective effect on depressive symptoms among older widowed women in South Korea.

Coresidence was found to be endogenous in our statistical model of depressive symptoms.

Discussion. The IV estimation method can be a useful approach to addressing the potential endogeneity between intergenerational coresidence and elderly health. Rapidly decreasing rates of intergenerational coresidence may raise public health concerns among older learn more selleck screening library widowed women in South Korea.”
“For over a decade, it has been known that amyloid beta (A beta) peptides of Alzheimer’s disease bind to the nicotinic alpha 7 acetylcholine receptor (AChR) with picomolar affinity, and that snake alpha-neurotoxins competitively inhibit this binding. Here we propose a model of the binding mechanism of A beta peptides to alpha 7-AChR at atomic level. The binding mechanism is based on sequence and structure similarities of A beta residues with functional

residues of snake alpha-neurotoxins (ATX) in complex with AChR. The binding mechanism involves residue (A beta)K28 (similar to (ATX)R32) which forms cation/pi interactions in the acetylcholine binding site, and residues (A beta)G29-(A beta)I32 [GAII] (similar to (ATX)G33-(ATX)I36 [GTII]) which form an intermolecular beta-sheet with residues (alpha 7)F189-(alpha 7)E191 of AChR. Through these interactions, we propose that the AChR serves as a chaperone for A beta conformational changes from alpha- to beta-hairpin. The interactions which block channel opening provide fundamental insight into A beta neurotoxicity and cognition impairment, that could contribute to pathogenic processes in Alzheimer’s disease, thus paving the way for structure based therapies.