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A qualitative tool was recently developed for evaluation of dependency in a demented population. This tool assesses the impact of cognitive impairment on functional status, taking into account disability in both the basic and the instrumental activities of daily living. The purpose of the present paper was to study the impact of dependency on informal caregivers who assist demented patients at home, with this new useful tool. Methods: A cross-sectional analysis was undertaken of the subgroup of 145 demented patients of the National Dementia Economic Study, aged ≥65 years, living in the community, with an available caregiver. A neuropsychological assessment of patients (Mini-Mental State Examination) and a comprehensive evaluation of caregivers (quality of life, Short Form Health Survey-36, depression, Sense of Competence) were recorded. A total of 32.4% were dependent, disabled in both basic and instrumental functions, 42.1% were non-dependent but with instrumental functional disabilities and 25.5% were non-dependent. Impact of dependency on the caregiver's experience was significant for different aspects (satisfaction with caregiving, subjective burden, quality of life, depression). Medical and non-medical costs increased with the severity of functional disability. Findings indicate that this tool is also useful to assess the impact of progression of functional disability in patients with dementia, on the caregiver issues. The consequences appeared both on personal feelings and on quality of life and financial involvement in management of the patient. Cognitive impairment appears to have more moderate repercussions in these areas. [ABSTRACT FROM AUTHOR]

Abstract: Activity-dependent neurotrophic factor (ADNF) and a 14-amino acid fragment of this peptide (sequence VLGGGSALLRSIPA) protect neurons from death associated with an array of toxic conditions, including amyloid β-peptide, N-methyl-d-aspartate, tetrodotoxin, and the neurotoxic HIV envelope coat protein gp120. We report that an even smaller, nine-amino acid fragment (ADNF9) with the sequence SALLRSIPA potently protects cultured embryonic day 18 rat hippocampal neurons from oxidative injury and neuronal apoptosis induced by FeSO4 and trophic factor withdrawal. Among the characteristics of this protection are maintenance of mitochondrial function and a reduction in accumulation of intracellular reactive oxygen species. [ABSTRACT FROM AUTHOR]

Noradrenergic neurons have been implicated in the development of ethanol dependence and tolerance. Moreover, the development of an hyposensltivity of alpha 2 adrenoceptors has been postulated during long-term exposition to ethanol. In order to test the putative role of alpha 2 receptors in ethanol intoxication, we have studied the interaction between ethanol and yohimbine, an alpha 2 antagonist, on the spontaneous firing rate of rat locus coeruleus (LC) in an in vitro slice model. The spikes from single neurons were recorded by glass microelectrodes. Ethanol at 100 mm, a concentration that parallels the behavioral effects in the human and in the animals, inhibits the firing activity of some LC cells. This inhibition was quickly reversed after stopping the ethanol perfusion and was observed for each further administration. However, if yohimbine (20 μm) was simultaneously perfused, the ethanol-induced inhibition was rapidly antagonized. This effect is reversible after long time washout of yohimbine. This suggests that alpha 2 adrenoceptors could beimplicated in the inhibitory effect of ethanol on LC noradrenergic neurons and perhaps inthe development of tolerance. However, other hypotheses are discussed, because yohimbine can also antag onize other types of receptors. [ABSTRACT FROM AUTHOR]

The article presents an abstract of the paper "Mechanisms of ADNF Peptide Protection Against Oxidative and Excitotoxic Neuronal Death," which will be presented at the 30th annual meeting of the American Society for Neurochemistry to be held from March 14-17, 1999 in New Orleans, Louisiana. The paper discusses how 9 amino acid fragment of activity-dependent neurotrophic factor peptide protects rat hippocampal neurons from oxidative injury and neuronal apoptosis.