SELECTED ABSTRACTS

DEPRESSION AFTER STROKE AND LESION LOCATION : A SYSTEMATIC REVIEW

ALAN J CARSON, SIOBHAN MACHALE, KATHRYN ALLEN, STEPHEN M LAWRIE, MARTIN DENNIS, ALLAN HOUSEM MICHAEL SHARPE
Background : There is conflicting evidence on the hypothesis that the risk of depression after stroke is influenced by the location of the brain lesion. We undertake a systematic review to examine the hypothesis that depression is more commonly associated with left hemisphere strokes than with right-hemisphere strokes and with lesions of the left anterior brain than with other regions.
Methods : We did a computer-aided search of MEDLINE, BIDS ISI, and PsychL it databases supplemented by hard searches of key journals. We included all reports on the  association of depression after stroke with the location of the brain lesion. Studies were systematically and independently examined by two investigators. Fixed- effects and random-effects meta-analysis were done.
 Finding 143 reports were identified by the search strategy. 48 were eligible for inclusion. Not all reports included original data. Only two reports of original data supported the hypothesis and seven clearly did not. The pooled (random effects) relative risk of depression after a left-hemisphere stroke, compared with a right-hemisphere stroke, was 0-95(95% Cl 0-83-1:10). For depression after a left anterior lesion compared with all other brain area the pooled (random effect) relative risk were 1:17(0.87-1.62). restriction of the analysis to reports from high0quality studies or major depressive disorder did not substantially affect the findings. Nor were they affected by stratification of the time between stoke and the assessment of depression. Multiple publications from the same samples of patients were apparent.
Interpretation : This systematic review offered no support for the hypothesis that the risk of depression after stroke as affected by the location of the brain lesion. The lancet 2000; 356: 122-126
ARE SCHIZOPHRENIC AND BIPOLAR DISORDER RELATED ? A REVIEW OF FAMILY AND MOLECULAR STUDIES
WADE H. BERRETTINI
Schizophrenic and bipolar disorders are similar in several epidemiologic respects, including age at onset, lifetime risk , course of illness, worldwide distribution, risk suicide, gender influence (men and women at equal risk for both groups of disorders), and genetic susceptibility. Despite these similarities, schizophrenia and bipolar disorders are typically considered to be separate entities, with distinguishing clinical characteristic, non-overlapping etiologies, and distinct treatment regimens. Over the past three decades, multiple family studies are consistent with greater nosologic overlap than previously acknowledged. Molecular linkage studies (conducted during the 1990s) reveal that some susceptibility loci may be common to both nosologic classes. This indicates that our nosology will require substantial revision during the next decade, to reflect this shared genetic susceptibility, as specific genes are identified. (Biol Psychiatry 2000; 48:531-538 2000 Society of Biological Psychiatry.) 

NIA NEWS : ALZHEIMER'S DISEASE RESEARCH UPDATE NASAL ALZHEIMER'S VACCINE SUCCESSFULLY TESTED IN MICE SEPTEMBER 28,2000
Nasal administration of synthetic beta amyloid peptide reduces potentially damaging Alzheimer's disease-like plaques in the brains of test mice and may one day be tested in clinical trails for its ability to vaccinate against plaque formation in people with Alzheimer's disease (AD), according to a new study by researchers at Harvard Medical School. The brains of the animals treated with the nasal spray had a significantly lower "plaque burden"..60 percent less in the hippocampus, for example---than mice that were not immunized or were treated with another protein, the scientists found. The findings are a significant step forward for the concept that an immunological approach, using vaccines, might one day be effective against Alzheimer's disease in humans.
 The research is a collaboration of the laboratories of Howard L. Weiner, M.D., and Dennis J Selkoe, M.D., at Harvard and Brigham and Women's Hospital. Cynthia Lemere, Ph.D., in the Selkoe group, and Ruth Maron, Ph.D., in the Weiner group, led the experiments. The findings are reported in the October 2000 issue of the Annals of Neurology. The national Institute on Aging (NIA) and the National Institute of Allergy and Infectious Disease (NIAID), both part of the Federal Government's National Institutes of Health, supported the study.
 This Annals report follows a 1999 report on an AD vaccine by Scientists at Elan Pharmaceuticals. In Elan's research, injections of the beta  amyloid peptide were shown to be effective in stopping the formation of the plaques in the same strain o mice that were used in the Harvard study, mice that were specially engineered to develop AD-like plaques. The company is now in the early stages of testing regular injections of an experimental beta amyloid vaccine for its safety in humans.
 This Harvard study delivered the beta-amyloid peptide nasally, using a method somewhat like the inhalers used to deliver allergy and asthma medicines. Scientists are interested in testing the delivery of the peptide nasally because it may be better tolerated in humans than repetitive injections over the long-term. In this study, the strength of antibodies resulting from nasal administration of the vaccine was not as great as that from the injection approach, although still significantly effective against plaque formation. The study also identified cellular immune responses in the brain of my treated nasally with amyloid with that may contribute to reducing plaque levels. Apart from the way the vaccine can lower plaque formation associated with AD.
 "This whole area of research Alzheimer's disease vaccines is extremely exiting", says D. Stephen Synder, Ph.D., who heads the Etiology of AD program at NIA. "There is a long way to go-likely".
 htt://www.alzheimers.org/nianews/nianews34.html