Mediterranean Diet and Stroke, Cognitive Impairment, Depression: A Meta-Analysis.

Mediterranean diet and stroke, cognitive impairment, depression: A meta-analysis.

Ann Neurol. 2013 May 30;
Psaltopoulou T, Sergentanis TN, Panagiotakos DB, Sergentanis IN, Kosti R, Scarmeas N

OBJECTIVE: This meta-analysis aims to quantitatively synthesize all studies that examine the association between adherence to a Mediterranean diet and risk of stroke, depression, cognitive impairment and Parkinson’s disease. METHODS: Potentially eligible publications were those providing effect estimates of relative risk (RR) for the association between Mediterranean diet and the aforementioned outcomes. Studies were sought in PubMed up to October 31, 2012. Maximally adjusted effect estimates were extracted; separate analyses were performed for high and moderate adherence. RESULTS: 22 eligible studies were included (11 for stroke, nine for depression and eight for cognitive impairment; only one pertained to Parkinson’s disease). High adherence to Mediterranean diet was consistently associated with reduced risk for stroke (RR=0.71, 95%CI: 0.57-0.89), depression (RR=0.68, 95%CI: 0.54-0.86) and cognitive impairment (RR=0.60, 95%CI: 0.43-0.83). Moderate adherence was similarly associated with reduced risk for depression and cognitive impairment, whereas the protective trend concerning stroke was only marginal. Subgroup analyses highlighted the protective actions of high adherence in terms of reduced risk for ischemic stroke, mild cognitive impairment, dementia and particularly Alzheimer’s disease. Meta-regression analysis indicated that the protective effects of Mediterranean diet in stroke prevention seemed more sizeable among males. Concerning depression, the protective effects of high adherence seemed independent of age, whereas the favorable actions of moderate adherence seemed to fade away along with older age. INTERPRETATION: Adherence to a Mediterranean diet may contribute to the prevention of a series of brain diseases; this may be of special value given the aging of Western societies. ANN NEUROL 2013. © 2013 American Neurological Association. HubMed – depression


Characterizing Social Behavior in Genetically Targeted Mouse Models of Brain Disorders.

Methods Mol Biol. 2013; 1017: 95-104
Burrows EL, Hannan AJ

Fragile X syndrome, the leading inherited cause of mental retardation and autism spectrum disorders worldwide, is caused by a tandem repeat expansion in the FMR1 (fragile X mental retardation 1) gene. It presents with a distinct behavioral phenotype which overlaps significantly with that of autism. Emerging evidence suggests that tandem repeat polymorphisms (TRPs) might also play a key role in modulating disease susceptibility for a range of common polygenic disorders, including the broader autism spectrum of disorders (ASD) and other forms of psychiatric illness such as schizophrenia, depression, and bipolar disorder [1]. In order to understand how TRPs and associated gene mutations mediate pathogenesis, various mouse models have been generated. A crucial step in such functional genomics is high-quality behavioral and cognitive phenotyping. This chapter presents a basic behavioral battery for standardized tests for assaying social phenotypes in mouse models of brain disorders, with a focus on aggression. HubMed – depression


Safety profile of antiviral medications: A pharmacovigilance study using the Italian spontaneous-reporting database.

Am J Health Syst Pharm. 2013 Jun 15; 70(12): 1039-1046
Pugi A, Bonaiuti R, Maggini V, Moschini M, Tuccori M, Leone R, Rossi M, Motola D, Piccinni C, Ferrazin F, Sottosanti L, Mugelli A, Vannacci A, Lapi F

PURPOSE: The results of an analysis of suspected antiviral-associated adverse drug reactions (ADRs) in Italy over a 22-year period are presented. METHODS: A case/non-case analysis was conducted using ADR reports compiled in the nationwide spontaneous-reporting database through September 2010. All reported events included in the analysis were evaluated and coded by drug safety experts; causality assessments were performed according to the algorithm of Naranjo et al. The association between an adverse reaction and antiviral use was assessed by estimating the reporting odds ratio (ROR), with 95% confidence interval (CI), as a measure of disproportionality. RESULTS: Overall, 863 reports of suspected ADRs involving antivirals and 42,430 reports of adverse reactions to other drugs were identified; of those events, 3.3% and 64.3% were determined to be definite or probable ADRs, respectively, and an additional 32.4% were deemed possibly drug related. Several ADRs were disproportionately associated with antivirals relative to other drugs: renal colic (ROR, 25.5; 95% CI, 13.3-49.0), lactic acidosis (ROR, 18.6; 95% CI, 9.2-37.7), depression (ROR, 18.0; 95% CI, 11.6-27.9), anemia (ROR, 15.9; 95% CI, 12.3-20.4), hallucination (ROR, 4.3; 95% CI, 2.7-7.1), neutropenia (ROR, 4.1; 95% CI, 2.9-5.8), acute renal failure (ROR, 3.9; 95% CI, 2.3-6.4), fever (ROR, 3.8; 95% CI, 2.8-5.1), hyperpyrexia (ROR, 2.9; 95% CI, 1.7-4.9), and asthenia (ROR, 1.8; 95% CI, 1.2-2.8). CONCLUSION: Analysis of data from a large Italian database showed that, among antiviral agents, the ribavirin-interferon combination, acyclovir, valacyclovir, indinavir, and zidovudine accounted for the most serious hematologic, neuropsychiatric, and renal ADRs. HubMed – depression


Long-Term Depression of Synaptic Kainate Receptors Reduces Excitability by Relieving Inhibition of the Slow Afterhyperpolarization.

J Neurosci. 2013 May 29; 33(22): 9536-9545
Chamberlain SE, Sadowski JH, Teles-Grilo Ruivo LM, Atherton LA, Mellor JR

Kainate receptors (KARs) are ionotropic glutamate receptors that also activate noncanonical G-protein-coupled signaling pathways to depress the slow afterhyperpolarization (sAHP). Here we show that long-term depression of KAR-mediated synaptic transmission (KAR LTD) at rat hippocampal mossy fiber synapses relieves inhibition of the sAHP by synaptic transmission. KAR LTD is induced by high-frequency mossy fiber stimulation and natural spike patterns and requires activation of adenosine A2A receptors. Natural spike patterns also cause long-term potentiation of NMDA receptor-mediated synaptic transmission that overrides the effects of KAR LTD on the cellular response to low-frequency synaptic input. However, KAR LTD is dominant at higher frequency synaptic stimulation where it decreases the cellular response by relieving inhibition of the sAHP. Thus we describe a form of glutamate receptor plasticity induced by natural spike patterns whose primary physiological function is to regulate cellular excitability. HubMed – depression



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