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Background: Primary Progressive Aphasia (PPA) involves an isolated impairment of language function at disease onset. The cholinergic system is implicated in language and cholinergic deficits are seen in brains of individuals with PPA. One major source of cholinergic innervation is the nucleus basalis of Meynert (NBM) within which lies the nucleus subputaminalis (NSP). We quantified cholinergic neurons in the NBM and NSP of PPA and controls. Also explored was whether individuals with PPA who subsequently developed different clinical and neuropathological profiles, showed similar cholinergic deficits in the NSP. Methods: Cytoarchitecture of the basal forebrain was studied using Nissl staining in control (n=5) and PPA (n=5) brains. Choline acetyltransferase immunohistochemical staining labelled cholinergic neurons, quantified using Neurolucida software. Results: Compared to matched controls, PPA showed reduction of cholinergic neurons in the NBM, t(4) = 4.224, p = 0.013; Cohen’s d=1.89 and the NSP, t(4) = 4.013, p = 0.016; Cohen’s d= 1.79. The average percent of cholinergic neuronal loss was higher in the NSP (64.66%) compared to NBM (17.66%). Conclusions: Regardless of underlying pathology, all cases presenting with PPA showed marked loss of cholinergic neurons in the NSP providing further evidence for the importance of this nucleus in language function.
Disturbances such as wildfire create time-sensitive windows of opportunity for invasive plant treatment, and the timing of herbicide application relative to the time course of plant community development following fire can strongly influence herbicide effectiveness. We evaluated the effect of herbicide (imazapic) applied in the first winter or second fall after the 113,000 ha Soda wildfire on the target exotic annual grasses and also key non-target components of the plant community. We measured responses of exotic and native species cover, species diversity, and occurrence frequency of shrubs and forbs seeded before (1 to 2 or 9 to 10 mo) herbicide application. Additionally, we asked whether landscape factors, including topography, species richness, and/or soil characteristics, influenced the effectiveness of imazapic. Cover of exotic annual grass cover, but not of deep-rooted perennial bunchgrass, was less where imazapic had been applied, whereas more variability was evident in the response of Sandberg bluegrass (Poa secunda J. Presl) and seeded shrubs and forbs. Regression-tree analysis of the subset of plots measured both before and after the second fall application revealed greater reductions of exotic annual grass cover in places where their cover was <42% before spraying. Otherwise, imazapic effects did not vary with the landscape factors we analyzed.
n-3 Fatty acids are associated with better cardiovascular and cognitive health. However, the concentration of EPA, DPA and DHA in different plasma lipid pools differs and factors influencing this heterogeneity are poorly understood. Our aim was to evaluate the association of oily fish intake, sex, age, BMI and APOE genotype with concentrations of EPA, DPA and DHA in plasma phosphatidylcholine (PC), NEFA, cholesteryl esters (CE) and TAG. Healthy adults (148 male, 158 female, age 20–71 years) were recruited according to APOE genotype, sex and age. The fatty acid composition was determined by GC. Oily fish intake was positively associated with EPA in PC, CE and TAG, DPA in TAG, and DHA in all fractions (P≤0·008). There was a positive association between age and EPA in PC, CE and TAG, DPA in NEFA and CE, and DHA in PC and CE (P≤0·034). DPA was higher in TAG in males than females (P<0·001). There was a positive association between BMI and DPA and DHA in TAG (P<0·006 and 0·02, respectively). APOE genotype×sex interactions were observed: the APOE4 allele associated with higher EPA in males (P=0·002), and there was also evidence for higher DPA and DHA (P≤0·032). In conclusion, EPA, DPA and DHA in plasma lipids are associated with oily fish intake, sex, age, BMI and APOE genotype. Such insights may be used to better understand the link between plasma fatty acid profiles and dietary exposure and may influence intake recommendations across population subgroups.
After the diagnosis of immune-mediated inflammatory diseases (IMID) such as inflammatory bowel disease (IBD), multiple sclerosis (MS) and rheumatoid arthritis (RA), the incidence of psychiatric comorbidity is increased relative to the general population. We aimed to determine whether the incidence of psychiatric disorders is increased in the 5 years before the diagnosis of IMID as compared with the general population.
Using population-based administrative health data from the Canadian province of Manitoba, we identified all persons with incident IBD, MS and RA between 1989 and 2012, and cohorts from the general population matched 5 : 1 on year of birth, sex and region to each disease cohort. We identified members of these groups with at least 5 years of residency before and after the IMID diagnosis date. We applied validated algorithms for depression, anxiety disorders, bipolar disorder, schizophrenia, and any psychiatric disorder to determine the annual incidence of these conditions in the 5-year periods before and after the diagnosis year.
We identified 12 141 incident cases of IMID (3766 IBD, 2190 MS, 6350 RA) and 65 424 matched individuals. As early as 5 years before diagnosis, the incidence of depression [incidence rate ratio (IRR) 1.54; 95% CI 1.30–1.84) and anxiety disorders (IRR 1.30; 95% CI 1.12–1.51) were elevated in the IMID cohort as compared with the matched cohort. Similar results were obtained for each of the IBD, MS and RA cohorts. The incidence of bipolar disorder was elevated beginning 3 years before IMID diagnosis (IRR 1.63; 95% CI 1.10–2.40).
The incidence of psychiatric comorbidity is elevated in the IMID population as compared with a matched population as early as 5 years before diagnosis. Future studies should elucidate whether this reflects shared risk factors for psychiatric disorders and IMID, a shared final common inflammatory pathway or other aetiology.
What do research psychologists do? How do they think about their work? What does psychological science look like as it goes on in the heads of top psychological scientists? How do these scientists develop their ideas over time?
The purpose of this book is to hear, in the first person, from some of the most eminent psychologists of the modern era regarding what they view as their single most important contribution to the behavioral and brain sciences. The list of invitees was based on rankings compiled by Diener, Shigehiro, and Park (2014), using criteria such as number of major awards, total number of citations, and pages of textbooks devoted to the scholars’ work. Such lists, of course, would have different members depending on the criteria used, but the list seemed to us as good a basis for recognition as any we could find.
We invited all living members of the list of 200 individuals (many were deceased at the time we were preparing the book) for whom we could find contact information. The overwhelming majority of individuals still living and able to write, 100 scientists in all, agreed to write either singly or jointly, yielding 101 chapters, including the introduction and conclusion. (Some individuals were still alive but no longer in sufficiently good health to be able to write a chapter.) In each case, they were given the option of either writing a sole-authored piece (which the large majority did), writing with another member of the list (which happened in two cases, in which the individuals became famous for their collaborative work), or writing with someone outside the list (which happened in one case, in which the junior author of the chapter was instrumental to the accomplishment of the work described). After asking each member of the list to write, we asked two additional extremely distinguished psychologists who are also academic leaders and administrators – a university president and a university chancellor – to write the foreword and afterword, and both agreed to do so.
Each essay addresses just five questions:
1. What do you consider to be your most important scientific contribution?
2. Why do you consider it to be your most important contribution?