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Specificity in Etiology of Subtypes of Bipolar Disorder: Evidence From a Swedish Population-Based Family Study.
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Specificity in Etiology of Subtypes of Bipolar Disorder: Evidence From a Swedish Population-Based Family Study.

Biol Psychiatry. 2017 Nov 20;:

Authors: Song J, Kuja-Halkola R, Sjölander A, Bergen SE, Larsson H, Landén M, Lichtenstein P

Abstract
BACKGROUND: Uncertainty remains whether bipolar I disorder (BDI) and bipolar II disorder (BDII) differ etiologically. We used a population-based family sample to examine the etiological boundaries between BDI and BDII by assessing their familial aggregation/coaggregation and by assessing the coaggregation between them and schizophrenia, depression, attention-deficit/hyperactivity disorder, eating disorders, autism spectrum disorder, substance use disorders, anxiety disorders, and personality disorders.
METHODS: By linking Swedish national registers, we established a population-based cohort (N = 15,685,511) and identified relatives with different biological relationships. Odds ratios (ORs) were used to measure the relative risk of BDI and BDII in relatives of individuals diagnosed with BDI (n = 4309) and BDII (n = 4178). The heritability for BDI and BDII and the genetic correlation across psychiatric disorders were estimated by variance decomposition analysis.
RESULTS: Compared with the general population, the OR of BDI was 17.0 (95% confidence interval [CI] 13.1-22.0) in first-degree relatives of BDI patients, higher than that of BDII patients (OR 9.8, 95% CI 7.7-12.5). The ORs of BDII were 13.6 (95% CI 10.2-18.2) in first-degree relatives of BDII patients and 9.8 (95% CI 7.7-12.4) in relatives of BDI patients. The heritabilities for BDI and BDII were estimated at 57% (95% CI 32%-79%) and 46% (95% CI 21%-67%), respectively, with a genetic correlation estimated as 0.78 (95% CI 0.36-1.00). The familial coaggregation of other psychiatric disorders, in particular schizophrenia, showed different patterns for BDI and BDII.
CONCLUSIONS: Our results suggest a distinction between BDI and BDII in etiology, partly due to genetic differences.

PMID: 29331354 [PubMed - as supplied by publisher]




Mechanisms of Sex Differences in Fear and Posttraumatic Stress Disorder.
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Mechanisms of Sex Differences in Fear and Posttraumatic Stress Disorder.

Biol Psychiatry. 2017 Nov 21;:

Authors: Ramikie TS, Ressler KJ

Abstract
Following sexual maturity, females disproportionately have higher rates of posttraumatic stress disorder (PTSD) and experience greater symptom severity and chronicity as compared with males. This observation has led many to examine sex differences in PTSD risk factors. Though relatively few, these studies reveal that the root causes of PTSD sex differences are complex, and partly represent interactions between sex-specific nonbiological and biological risk factors, which differentially shape PTSD vulnerability. Moreover, these studies suggest that sex-specific PTSD vulnerability is partly regulated by sex differences in fear systems. Fear, which represents a highly conserved adaptive response to threatening environmental stimuli, becomes pathological in trauma- and stress-based psychiatric syndromes, such as PTSD. Over the last 30 years, considerable progress has been made in understanding normal and pathological molecular and behavioral fear processes in humans and animal models. Thus, fear mechanisms represent a tractable PTSD biomarker in the study of sex differences in fear. In this review, we discuss studies that examine nonbiological and biological sex differences that contribute to normal and pathological fear behaviors in humans and animal models. This, we hope, will shed greater light on the potential mechanisms that contribute to increased PTSD vulnerability in females.

PMID: 29331353 [PubMed - as supplied by publisher]




Prion Protein as a Toxic Acceptor of Amyloid-β Oligomers.
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Prion Protein as a Toxic Acceptor of Amyloid-β Oligomers.

Biol Psychiatry. 2018 Feb 15;83(4):358-368

Authors: Purro SA, Nicoll AJ, Collinge J

Abstract
The initial report that cellular prion protein (PrPC) mediates toxicity of amyloid-β species linked to Alzheimer's disease was initially treated with scepticism, but growing evidence supports this claim. That there is a high-affinity interaction is now clear, and its molecular basis is being unraveled, while recent studies have identified possible downstream toxic mechanisms. Determination of the clinical significance of such interactions between PrPC and disease-associated amyloid-β species will require experimental medicine studies in humans. Trials of compounds that inhibit PrP-dependent amyloid-β toxicity are commencing in humans, and although it is clear that only a fraction of Alzheimer's disease toxicity could be governed by PrPC, a partial, but still therapeutically useful, role in human disease may soon be testable.

PMID: 29331212 [PubMed - in process]




Emerging Mechanisms in Alzheimer's Disease and Their Therapeutic Implications.
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Emerging Mechanisms in Alzheimer's Disease and Their Therapeutic Implications.

Biol Psychiatry. 2018 Feb 15;83(4):298-299

Authors: Strittmatter SM

PMID: 29331211 [PubMed - in process]