There has been continued interest in the nature of the association between affective disorders and alcoholism. This may be due to the fact that during the course of alcoholism 30-70% of the patients suffer from mood disturbances meeting the criteria for severe depression, especially in periods of excessive alcohol consumption or during withdrawal. In the course of a prospective multidimensional study, Tiibinger Alkoholismusprojekt (T-ALK Study), symptoms of depression in 31 male alcohol-dependent patients (RDC diagnosis) were assessed using the Beck Depression Inventory (BDI) and the Freiburger Personlichkeitsinventar (FPI-R) at the beginning and at the end of a 6-week inpatient treatment program. There was only a moderate degree of depression (BDI) in 20% of the patients which decreased significantly during the psychotherapeutic treatment under conditions of confirmed abstinence. No correlations between the degree of depression and neuropsychological impairment were found. Although the “satisfaction with life” (FPI-R factor) was still impaired in a third of the patients at the end of that short-term treatment period, our results do not indicate a general nosological overlap between alcoholism and affective disorders in males.

Measures of brain and hippocampal volume in 40 healthy young (aged 18–30 years) and 36 healthy elderly (aged 60–83 years) subjects were compared with composite cognitive function scores in three conceptual domains: memory ability, processing speed, and general fluid intelligence. Through a series of general linear models testing the relationship between these brain measures and cognitive performance scores, a significant positive relationship between hippocampal volume and fluid intelligence ability was found in elderly subjects but not in young. No relationship between the other cognitive domains and brain or hippocampal volume was found. The findings suggest a role of hippocampal atrophy in the decline in fluid intelligence in the elderly. (JINS, 2011, 17, 000–000)

Background: Plasma homocysteine has been associated with reduced brain volumes in cross-sectional studies. We aimed to investigate if homocysteine is associated with ongoing atrophy, and if so, if this is localized to gray or white matter.

Methods: In a group of 80 hypertensive subjects aged 70–90 years (from the SCOPE study) MRI images were obtained at two time points two years apart. Rates of gray and white matter and hippocampal atrophy were determined by calculating the difference in segmentation probability maps using SPM5. Plasma homocysteine, folate, B12 and creatinine were measured at study end.

Results: Homocysteine levels correlated with white matter atrophy rate (p = 0.006) hippocampal baseline volume (p = 0.011) and hippocampal atrophy rate (p = 0.004) but not global gray matter atrophy or baseline gray or white matter volumes. The correlations remained significant (p < 0.05) after controlling for subject age, blood pressure, folate levels and white matter lesion volume.

Conclusion: In older hypertensives, plasma homocysteine levels are associated with increased rates of progressive white matter and hippocampal atrophy.

Background: Brain atrophy in Alzheimer's disease (AD) includes not only AD-specific brain atrophy but also the atrophy induced by normal aging. Atrophy of the hippocampus has been one diagnostic marker of AD, but it was also found to emerge in healthy adults, along with increasing age. It was reported that the important age when age-related shrinkage of the hippocampus starts was around the mid-40s. The aim is to study the aging atrophy speed and acceleration of brain atrophy in a cross-sectional database, to identify the age at which acceleration of hippocampal atrophy starts in non-demented elderly persons.

Methods: 544 subjects (aged 60–97 years; 318 female and 226 male) were recruited into the MRI study by using a subsample of an epidemiological sample of 3363 healthy non-demented elderly people (over 60 years of age). Hippocampus and ventricle sizes were measured.

Results: The normalized volumes (by intracranial volume, ICV) of the hippocampus in males were smaller than those in females. The right hippocampus was larger than the left. The expansion of the lateral ventricles (2.80% per year in males, 2.95% in females) and third ventricle (1.58% and 2.28%, respectively) was more marked than the hippocampal shrinkage (0.68% and 0.79%, respectively). The suggested age at which acceleration of hippocampal atrophy starts is 72 years.

Conclusions: Males present smaller hippocampus volumes (normalized by ICV) than females; however, females are more vulnerable to hippocampal atrophy in a non-demented elderly population. An acceleration of hippocampal atrophy may emerge and start around 72 years of age in a non-demented elderly population.

According to the cognitive reserve hypothesis, neuropsychological expression of brain disease is attenuated among persons with higher education or premorbid intelligence. The current research examined cognitive reserve in multiple sclerosis (MS) by investigating whether the negative effect of brain atrophy on information processing (IP) efficiency is moderated by premorbid intelligence. Thirty-eight persons with clinically definite MS completed a vocabulary-based estimate of premorbid intelligence (Wechsler Vocabulary) and a composite measure of IP efficiency (Symbol Digit Modalities Test and Paced Auditory Serial Addition Task). Brain atrophy was estimated from measurements of third ventricle width using high-resolution anatomical brain magnetic resonance imaging (magnetization-prepared rapid gradient echo). In a hierarchical regression analysis controlling for age and depressive symptomatology, brain atrophy predicted worse IP efficiency (R2 = .23, p = .003) and cognitive reserve predicted better IP efficiency (R2 = .13, p = .013), but these effects were moderated by an Atrophy × Cognitive Reserve interaction (R2 = .15, p = .004). The negative effect of brain atrophy on IP efficiency was attenuated at higher levels of reserve, such that MS subjects with higher reserve were better able to withstand MS neuropathology without suffering cognitive impairment. Results help explain the incomplete and inconsistent relationship between brain atrophy and IP efficiency in previous research. (JINS, 2009, 15, 606–612.)

The regional distribution of degeneration of the corpus callosum (CC) in dementia is not yet clear. This study compared regional CC size in participants (n = 179) from the Cache County Memory and Aging Study. Participants represented a range of cognitive function: Alzheimer's disease (AD), vascular dementia (VaD), mild ambiguous (MA–cognitive problems, but not severe enough for diagnosis of dementia), and healthy older adults. CC outlines obtained from midsagittal magnetic resonance images were divided into 99 equally spaced widths. Factor analysis of these callosal widths identified 10 callosal regions. Multivariate analysis of variance revealed significant group differences for anterior and posterior callosal regions. Post-hoc pairwise comparisons of CC regions in patient groups as compared to the control group (controlling for age) revealed trends toward smaller anterior and posterior regions, but not all were statistically significant. As compared to controls, significantly smaller anterior and posterior CC regions were found in the AD group; significantly smaller anterior CC regions in the VaD group; but no significant CC regional differences in the MA group. Findings suggest that dementia-related CC atrophy occurs primarily in the anterior and posterior portions. (JINS, 2008, 14, 414–423.)

HIV infection often results in MRI-detectable brain atrophy and white matter signal hyperintensities (WMSHs). Magnetic resonance images were obtained from 31 HIV+ male patients and 10 high-risk controls. Variation within the HIV+ group on neuropsychological (NP) impairment and stage of systemic disease were relatively independent, allowing examination of the relative association of MRI measures with NP impairment versus with systemic stage of disease. HIV+ patients compared to high-risk controls evidenced global atrophy, reduced caudate nuclei volume, and a trend to gray matter volume loss but no difference in white matter volume or in WMSHs. These effects were progressive with CDC clinical stage such that patients at CDC stage A had values very close to those of controls, while patients at CDC stage C had the most abnormal values. In contrast, the relationship between these MRI variables and severity of NP impairment was much less dramatic, with the mildly to moderately impaired HIV+ subjects showing MRI volume effects greater than or equal to those of the severely impaired HIV+ subjects. These results suggest that MRI-detectable brain atrophy secondary to HIV infection is not the primary substrate underlying the progressive NP impairment in HIV disease. (JINS, 1997, 3, 276–287.)