Faculty Bibliography

Background: Subjective Cognitive Impairment (SCI), Global Deterioration Scale stage 2, is common in older persons. A study of otherwise healthy persons found that 54% of SCI subjects followed over 7 years progressed toMild Cognitive Impairment (MCI) or dementia (Reisberg, et al., Alzheimer's & Dementia, 2010).1 Medications may contribute to SCI occurrence, however, their influence on SCI outcome is largely unknown. Therefore, we investigated the impact of medications subsequently associated with dementia risk in our previously characterized cohort.1 Methods: Subjects with SCI at baseline from our 2010 publication1 were studied. These subjects had baseline evaluations between 1/1/1984 and 12/31/1997 and were followed until 12/31/2001. Medication data was available on 143 of 166 subjects. Subjects receiving topical estrogen at the baseline evaluationwere excluded fromthese analyses. At baseline, evaluable subjects (N = 140; 91 women, 49 men) had a mean age of 66.5 +/- 8.4 years; 15.6 +/- 2.7 years of education; and MMSE scores of 29.0 +/- 1.2. Twenty-two women (24.2%) were receiving HRT, comprising estrogen (n = 10) or estrogen-progesterone combination (n = 12). Results: Subjects were followed over 7.0 +/- 3.4 years. Increased age and education were associated with clinical progression in this cohort (OR = 1.06 and 0.78 respectively; p-values < 0.05). Three of ten estrogenonly (30%) subjects progressed (2 to MCI, 1 to dementia); seven of twelve estrogen-progesterone (58.3%) subjects progressed (6 toMCI, 1 to dementia). In the total HRT group, 45.5% progressed, whereas in the control group (no-HRT), 62 of 118 progressed (52.5%), (49 to MCI, 13 to dementia). Age, education and gender did not differ significantly between subjects in the study groups (t-test and chi-square p-values, NS). Multivariate logistic regression for each condition was performed investigating differences in therapy, age, gender and education. Therapy was not associated with progression status. Conclusions: HRT did not influence 7-year outcome in SCI subjects. Therefore, SCI subjects were not particularly sensitive to reported deleterious effects of HRT on progression of cognitive decline. Systematic longitudinal investigation of possible effects of other medications/conditions on progression of SCI to MCI/dementia is required to identify substances that may regulate/prevent this process

Tardive dyskinesia (TD) is a severe and potential irreversible side effect of antipsychotic treatment. Treatment of established TD is often unsuccessful. In this article, we report three cases of psychogeriatric patients who suffered from TD as a side effect of long-term treatment with haloperidol that resolved after switching treatment to aripiprazole. Potential psychopharmacological mechanisms explaining this finding are briefly discussed

Early diagnosis of Alzheimer disease (AD) is one of the major challenges for the prevention of this dementia. The pathologic lesions associated with AD develop many years before the clinical manifestations of the disease become evident, during a likely transitional period between normal aging and the appearance of first cognitive symptoms. AD biomarkers are needed not only to reveal these early pathologic changes but also to monitor progression in cognitive and behavioral decline and brain lesions. PET neuroimaging can reliably assess indirect and direct aspects of the molecular biology and neuropathology of AD. This article reviews the use of [18F] 2-fluoro-2-deoxy-D-glucose-PET and amyloid PET imaging in the early detection of AD.

Preclinical diagnosis of Alzheimer's disease (AD) is one of the major challenges for the prevention of AD. AD biomarkers are needed not only to reveal preclinical pathologic changes, but also to monitor progression and therapeutics. PET neuroimaging can reliably assess aspects of the molecular biology and neuropathology of AD. The aim of this article is to review the use of FDG-PET and amyloid PET imaging in the early detection of AD.

BACKGROUND:Depression is the most frequent psychiatric disorder in the elderly. Some authors consider late onset depression as a partially different phenomenological entity from that of the adult depression. The reason is its frequent association to dysexecutive cognitive impairment and cardiovascular risk factors. OBJECTIVE:This study aimed to analyze cognitive performance in neuropsychological screening tests in a group of late onset depression patients and non-depressed older adults. METHODS:Data was analyzed from 20 adults >or= 60 years old with late-life depression in partial or total remission and 10 individuals with the same characteristics but without previous affective disorders. Data was gathered on age, gender, education level, medical and psychiatric history and pharmacological history. Overall cognitive functions, executive performances, depressive symptoms, vascular risk factors and comorbid medical illness were measured using standardized test such as the Mini-mental State Examination (MMSE), Executive Interview (EXIT-S), Geriatric Depression Scale (GDS), Cumulative Illness Rating Scale (CIRS). The differences between groups were analyzed with Analysis of Variance (ANOVA). RESULTS:Patients with late-onset depression had statistically significant greater executive difficulties regarding the control group on the EXIT-S scale. CONCLUSIONS:Executive dysfunction can be considered a biological marker of late-life depression, although studies in larger samples of patients are needed.