Daniel David

Abstract

Objectives: With the worldwide population growing in age, information technology may help meet important needs to prepare and support patients and families for aging. We sought to explore the use and acceptance of information technology for health among the elderly by reviewing the existing literature. Methods: Review of literature using PubMed and Google Scholar, references from relevant papers, and consultation with experts. Results: Elderly people approach the Internet and health information technology differently than younger people, but have growing rates of adoption. Assistive technology, such as sensors or home monitors, may help 'aging in place', but these have not been thoroughly evaluated. Elders face many barriers in using technology for healthcare decision-making, including issues with familiarity, willingness to ask for help, trust of the technology, privacy, and design challenges. Conclusions: Barriers must be addressed for these tools to be available to this growing population. Design, education, research, and policy all play roles in addressing these barriers to acceptance and use.

Abstract

This project used the interRAI based, community health assessment (CHA) to develop a model for identifying current elder drivers whose driving behavior should be reviewed. The assessments were completed by independent housing sites in COLLAGE, a non-profit, national senior housing consortium. Secondary analysis of data drawn from older adults in COLLAGE sites in the United States was conducted using a baseline assessment with 8042 subjects and an annual follow-up assessment with 3840 subjects. Logistic regression was used to develop a Driving Review Index (DRI) based on the most useful items from among the many measures available in the CHA assessment. Thirteen items were identified by the logistic regression to predict drivers whose driving behavior was questioned by others. In particular, three variables reference compromised decision-making abilities: general daily decisions, a recent decline in ability to make daily decisions, and ability to manage medications. Two additional measures assess cognitive status: short-term memory problem and a diagnosis of non-Alzheimers dementia. Functional measures reflect restrictions and general frailty, including receiving help in transportation, use of a locomotion appliance, having an unsteady gait, fatigue, and not going out on most days. The final three clinical measures reflect compromised vision, little interest or pleasure in things normally enjoyed, and diarrhea. The DRI focuses the review process on drivers with multiple cognitive and functional problems, including a significant segment of potentially troubled drivers who had not yet been publicly identified by others. There is a need for simple and quickly identified screening tools to identify those older adults whose driving should be reviewed. The DRI, based on the interRAI CHA, fills this void. Assessment at the individual level needs to be part of the backdrop of science as society seeks to target policy to identify high risk drivers instead of simply age-based testing.

Abstract

The present study was undertaken to investigate the effects of bone morphogenetic protein-7 (BMP-7), also named osteogenic protein-1 (OP-1), on the progression of a striatal 6-hydroxydopamine (6-OHDA) lesion. BMP-7, a member of the transforming growth factor-β (TGF-β) superfamily of proteins, has been shown to have protective effects in other animal models of neuronal damage. In this study, male Fischer 344 rats received striatal 6-OHDA lesions followed 1 week later by an intraventricular dose of BMP-7. No significant effect of BMP-7 treatment on spontaneous locomotor activity was observed, however BMP-7 significantly increased the density of tyrosine hydroxylase (TH) immunoreactivity (TH-ir) in the substantia nigra (SN) pars compacta, in the lesioned hemisphere [31.7±5.2 (optical density (O.D.) arbitrary units) control vs. 50.2±4.3 O.D. BMP-7-treated; p<0.05]. Interestingly, BMP-7 significantly increased TH-ir in the SN of the non-lesioned hemisphere (pars reticulata: 14.8±1.19 O.D. control vs. 36±2.6 O.D. BMP-7-treated, p<0.05; pars compacta: 29.0±4.9 O.D. control vs. 64.4±6.9 O.D. BMP-7-treated, p<0.001). A significant increase in DA concentration in the contralateral, non-lesioned hemisphere was also noted (113.2 ng/g control vs. 198.2 ng/g BMP-7-treated, p<0.01). In contrast to other intraventricularly administered neurotrophic factors, BMP-7 was not associated with an increase in the sensitivity to pain. These results suggest that BMP-7 is able to act as a dopaminotrophic agent without unwanted side effects and as such may be a useful pharmacological tool in the treatment of Parkinson's disease in humans.

Abstract

The dopamine (DA) uptake/clearance properties of the DA transporter (DAT) in the core and shell of the nucleus accumbens were measured using in vivo electrochemical recordings. Calibrated amounts of a DA solution were pressure-ejected from a micropipette/ electrode assembly placed in the core or shell of the nucleus accumbens in anesthetized male Fischer 344 rats. Initial studies in the two brain regions revealed that the core and shell have different DA clearance properties as measured by the extracellular DA signal amplitudes, clearance times, and clearance rates. Although the same number of picomoles of DA were applied, DA clearance signals recorded in shell had significantly greater amplitudes but faster clearance rates than those recorded in the core. Systemic administration of 20 mg/kg cocaine, a monoamine transporter inhibitor, greatly increased the signal amplitude from the locally applied DA in both the core and shell. Signal amplitudes were increased to a greater extent in the shell, compared with the core, after cocaine administration. However, cocaine affected the clearance time of DA only in the core and the DA clearance rate only in the shell. Taken together with previously reported data, these studies further support differential activity of the DAT in the core versus shell subregions of the nucleus accumbens. In addition, these data indicate that DATs are more sensitive to the effects of psychomotor stimulants, such as cocaine, in the shell of the nucleus accumbens.

Abstract

The effects of cholinergic agonists on nitric oxide (NO) release in hippocampal slices from male Sprague-Dawley rats were investigated using electrochemical recording procedures using Nafion and o-phenylenediamine- treated carbon fiber microelectrodes. These microelectrodes are highly selective for NO versus other interferents. Acetylcholine (Ach) with neostigmine, or nicotine was delivered by pressure ejection from pipettes placed within 300 μm of the NO sensors. Both Ach arid nicotine produced NO signals ranging from 0.04 to 2.14 μM in the CA1, CA3, and dentate gyrus of the rat hippocampus that lasted for 2-5 min. The Ach responses were not antagonized by the muscarinic antagonist atropine. However, nicotine-evoked responses were partially antagonized by α-bungarotoxin, a finding consistent with α7-nicotinic cholinergic receptors being involved with the effects of nicotine. These data support the hypothesis that nicotine is capable of evoking long lasting NO release in the hippocampus.

Abstract

Intraparenchymal injections of the neurotoxin 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle in rats destroys the dopaminergic neurons in the pars compacta of the substantia nigra. In other transmitter systems it has been found that axotomy or neurotoxin exposure produces an initial loss of neurotransmitter phenotype, with cell death occurring over a much slower time course. To determine whether this also occurs in dopamine neurons after 6-OHDA, two approaches were utilized. First, the effect of injections of 6-OHDA into the medial forebrain bundle on nigral dopaminergic neurons was studied using combined fluorogold and immunocytochemical labeling. Four weeks after the 6-OHDA injection, there was an 85% reduction in the number of tyrosine hydroxylase (TH)-immunoreactive cells on the lesioned side. In contrast, there was only a 50% reduction in the number of fluorogold-labeled cells on the lesioned side. Second, the time course of the rescue of dopaminergic neurons after 6-OHDA by glial cell line-derived neurotrophic factor (GDNF) was determined using TH immunocytochemistry. Greater numbers of dopamine neurons were rescued 9 weeks after GDNF compared with counts made 5 weeks after GDNF. Taken together, these results suggest loss of dopaminergic phenotype is greater than cell loss following 6-OHDA injections, and that GDNF restores the phenotype of affected cells.