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Biomedical subjects

Glen L Xiong

Publications and source records attributed to Glen L Xiong.

6 recordsLinked to original sources
PubMed2007

Bupropion for weight reduction.

Bupropion is a norepinephrine and dopamine uptake inhibitor that has been available for several years for the treatment of depression and aiding smokers to quit. Although bupropion is not approved for treating obesity, three randomized clinical trials have shown some degree of efficacy for this drug in promoting weight loss in obese patients. The present drug profile provides a review of the pharmacology of bupropion, clinical evidence of efficacy with regard to weight reduction, tolerability and risks, and the current and future role of this drug in the management of obesity.

Antidepressive Agents, Second-Generation↗
PubMed2006

Vascular risk factors and cognitive decline among elderly male twins.

BACKGROUND: Studies investigating the association between cardiovascular risk factors and cognitive decline report discrepant outcomes. The co-twin control method improves on traditional case-control approaches by controlling for within-twin pair similarities of genetic and early environmental influences. OBJECTIVE: To examine the association of diabetes, hypertension, hypercholesterolemia, and elevated body mass index (BMI) (>30 kg/m(2)), individually and combined, with cognitive decline over a 12-year period in members of the National Academy of Sciences-National Research Council Twin Registry of World War II male veterans. METHODS: Modified Telephone Interview for Cognitive Status (TICS-m) was administered four times at approximately 4-year intervals from 1990 to 2002 as part of an epidemiologic study of dementia. Self-report medical information was collected from 1996 to 2002. We examined the difference in cognitive decline within twin pairs discordant for the vascular risk factors while controlling for baseline TICS-m, education, smoking, and alcohol history. RESULTS: Among twin pairs discordant for diabetes (n = 177), the diabetic twins declined an average of almost 1 point more than their nondiabetic co-twins (p = 0.018) at the last screening time point. Further analyses showed that this was in large part due to greater decline among older men (age 76 to 84 years). Cognitive change was not significantly different between members of pairs discordant for hypertension (n = 326), hypercholesterolemia (n = 282), or elevated BMI (n = 166). CONCLUSION: Based on this study of twin pairs who share similar genetic and early environmental risks for cardiovascular risk factors, diabetes is associated with greater cognitive decline, particularly among the oldest individuals.

Age Factors↗
PubMed2006

Prognosis of patients taking selective serotonin reuptake inhibitors before coronary artery bypass grafting.

Depression is increasingly recognized as an independent prognostic risk factor in patients with coronary artery disease and coronary artery bypass grafting (CABG). The use of selective serotonin reuptake inhibitors (SSRIs) for depression in patients with cardiac disease is becoming more prevalent. We examined the long-term outcomes of patients on SSRIs before CABG. We prospectively examined collected data in the Duke Databank for Cardiovascular Disease from January 1, 1999 to December 31, 2003. The median and maximum follow-up periods were 3 and 6 years, respectively. We screened patients who underwent CABG (n = 5,364) and excluded those who underwent simultaneous CABG and valvular surgery (n = 570). SSRI antidepressants included fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, escitalopram, venlafaxine, and clomipramine, and their use was determined from the inpatient pharmacy records during the index hospitalization. Outcomes included event-free survival from all-cause mortality, rehospitalization, and a composite end point of all-cause mortality or rehospitalization. Of 4,794 CABG-only patients, 246 (5.1%) took SSRIs before CABG. The SSRI group had a higher prevalence of diabetes, hypercholesterolemia, hypertension, cerebrovascular disease, peripheral vascular disease, and previous cardiovascular intervention. After adjustment for baseline differences, patients on SSRIs before CABG had increased risks of mortality, rehospitalization, and the composite end point (hazard ratio 1.61, 95% confidence interval 1.17 to 2.21, p = 0.003; hazard ratio 1.52, 95% confidence interval 1.30 to 1.77, p <0.0001; and hazard ratio 1.46, 95% confidence interval 1.26 to 1.70, p <0.0001, respectively). In conclusion, SSRI use before CABG was associated with a higher risk of long-term post-CABG mortality and rehospitalization. The explanation behind these findings requires further research.

Aged↗
PubMed2006

Pharmacological strategies for the prevention of Alzheimer's disease.

This review examines key pharmacological strategies that have been clinically studied for the primary or secondary prevention of Alzheimer's disease. Much information (neuropsychological, genetic and imaging) is already available to characterise an individual's risk for developing Alzheimer's disease. However, regulatory pathways for obtaining a prevention indication are less well charted, and such trials tend to involve 3- to 7-year studies of 1000 - 5000 individuals, depending on baseline status. Treatments developed for prevention will also need to have superior safety. For these reasons, > 100 proprietary pharmacological products are currently being developed for an Alzheimer's disease treatment, but only a few are being studied for prevention. Randomised trial data are available for antihypertensive agents (calcium channel blockers, angiotensin-converting enzyme inhibitors), pravastatin, simvastatin, conjugated oestrogen, raloxifene, rofecoxib, CX516 (AMPA agonist) and cholinesterase inhibitors regarding efficacy for Alzheimer's disease prevention. At least four large prevention trials of conjugated oestrogen, selenium and vitamin E, Ginkgo biloba and statins are currently underway. Strategies using other agents have not yet been evaluated in Alzheimer's disease prevention clinical trials. These include anti-amyloid antibodies, active immunisation, selective secretase inhibitors and modulators, microtubule stabilisers (e.g., paclitaxel), R-flurbiprofen, xaliproden, ONO-2506, FK962 (somatostatin releaser), SGS 742 (GABA(B) antagonist), TCH 346 (apoptosis inhibitor), Alzhemedtrade mark, phophodiesterase inhibitors, rosiglitazone, leuprolide, interferons, metal-protein attenuating compounds (e.g., PBT2), CX717, rasagaline, huperzine A, antioxidants and memantine. Studies combining lifestyle modification and drug therapy have not been conducted. Full validation of surrogate markers for disease progression (such as amyloid imaging) should further facilitate drug development. Reducing the complexity of prevention trials and gaining regulatory consensus of design is a high priority for the field.

Alzheimer Disease↗
PubMed2005

Statins and cognition: what can we learn from existing randomized trials?

BACKGROUND: Statins are being developed as treatments for Alzheimer's dementia based on evidence from preclinical and observational studies. However, cholesterol plays an integral role in cell membrane signal transduction and suboptimal cholesterol level could potentially impair neuronal function. Additionally, results of observational nonrandomized studies may have been affected by treatment bias. METHODS: We performed a systematic literature review in MEDLINE from January 1966 to July 2004 and included published prospective, randomized, and placebo-controlled human studies that examined the cognitive effects of statins. RESULTS: Nine studies with sample sizes ranging from 22 to 20,000 and duration of 3 weeks to 5 years, met criteria for review. Study populations and cognitive outcomes varied. Four studies were >6 months or longer. Overall, none of these studies reported finding a positive benefit for any statin on cognition in non-demented subjects although there was inconsistent evidence for acute cognitive worsening in some studies. CONCLUSION: While statins intuitively have appeal for the prevention or treatment of dementia, any conclusions about their efficacy should await more definitive evidence from on-going prospective clinical trials.

Alzheimer Disease↗