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Children born prematurely exhibit a broad range of neuroanatomical abnormalities. The aim of this study was to investigate the long-term effects of very preterm birth on brain volume (cortical and subcortical), cortical thickness and surface area. The participants were 25 children born very preterm (<32 weeks gestational age) without significant post-natal medical sequelae and 32 term-born children between 7 and 10 years of age. Neuroanatomical measures were derived from an automated pipeline. The results suggest a pattern of decreased brain volume, surface area and cortical thickness for children born preterm and the relation between subcortical gray volume and total brain volume differed between groups. The cortex was significantly thinner for children born preterm than term-born children in focal regions of the parietal and temporal lobes. Therefore, even without significant postnatal medical sequelae, very preterm children still exhibit structural differences that persist into middle childhood.

Children born prematurely exhibit a broad range of neuroanatomical abnormalities. The aim of this study was to investigate the long-term effects of very preterm birth on brain volume (cortical and subcortical), cortical thickness and surface area. The participants were 25 children born very preterm (<32 weeks gestational age) without significant post-natal medical sequelae and 32 term-born children between 7 and 10 years of age. Neuroanatomical measures were derived from an automated pipeline. The results suggest a pattern of decreased brain volume, surface area and cortical thickness for children born preterm and the relation between subcortical gray volume and total brain volume differed between groups. The cortex was significantly thinner for children born preterm than term-born children in focal regions of the parietal and temporal lobes. Therefore, even without significant postnatal medical sequelae, very preterm children still exhibit structural differences that persist into middle childhood.

Social isolation is commonly reported in individuals with isolated cleft lip and palate (ICLP), and is often cited as due to secondary factors of living with a facial malformation. However, the data are mixed, and the literature is biased to self-report studies. This study aimed to go beyond self-report data, and various components of social functioning were examined in a group of males with and without ICLP. The main aim of the study was to assess and compare social motivation in ICLP, and to relate social adjustment to brain structure. It was predicted that males with ICLP would be more likely to be socially isolated; however, self-concept was predicted to be similar to the comparison group (NC). Additionally, males with ICLP were predicted to have reduced social motivation (i.e., social abulia). Finally, volumes of the medial orbitofrontal cortex (mOFC) and the cerebellum were predicted to be related to social outcomes. The sample's age range was 13 - 25 years old, and 20 males with ICLP were compared to a group of 20 NC males. MRI scans were obtained from all the participants. As expected, males with ICLP were more likely to be socially isolated. Against predictions, they also had lower self-concept relative to the NC group. However, self-concept was not related to the extent of facial abnormality in the ICLP group. In line with predictions, the study did provide evidence for social abulia as a mechanism for social isolation, as males with ICLP had a more positive attitude after being socially excluded relative to excluded NC males. Unexpectedly however, the groups responded the same to social pressure, as all participants were more likely to take riskier turns in a driving simulator experiment when someone behind them was honking. Finally, social adjustment was significantly correlated with the volume of the mOFC, and posterior cerebellum white matter. Both correlations suggested that individuals with larger volumes were more likely to be better socially adjusted. In conclusion, the study provided evidence for a potentially different mechanism of social isolation in ICLP, and showed that brain morphology may at least partly underlie social dysfunction as well.

Background: Anorexia nervosa (AN) is characterized by sizable, widespread gray matter (GM) reductions in the acutely underweight state. However, evidence for persistent alterations after weight-restoration has been surprisingly scarce despite high relapse rates, frequent transitions to other psychiatric disorders, and generally unfavorable outcome. While most studies investigated brain regions separately (univariate analysis), psychiatric disorders can be conceptualized as brain network disorders characterized by multivariate alterations with only subtle local effects. We tested for persistent multivariate structural brain alterations in weight-restored individuals with a history of AN, investigated their putative biological substrate and relation with 1-year treatment outcome. Methods: We trained machine learning models on regional GM measures to classify healthy controls (HC) (N = 289) from individuals at three stages of AN: underweight patients starting intensive treatment (N = 165, used as baseline), patients after partial weight-restoration (N = 115), and former patients after stable and full weight-restoration (N = 89). Alterations after weight-restoration were related to treatment outcome and characterized both anatomically and functionally. Results: Patients could be classified from HC when underweight (ROC-AUC = 0.90) but also after partial weight-restoration (ROC-AUC = 0.64). Alterations after partial weight-restoration were more pronounced in patients with worse outcome and were not detected in long-term weight-recovered individuals, i.e. those with favorable outcome. These alterations were more pronounced in regions with greater functional connectivity, not merely explained by body mass index, and even increases in cortical thickness were observed (insula, lateral orbitofrontal, temporal pole). Conclusions.: Analyzing persistent multivariate brain structural alterations after weight-restoration might help to develop personalized interventions after discharge from inpatient treatment.

Humans have an innate ability to deal with numerosity and other aspects of magnitude. This ability is generally honed through education in and experience with mathematics, which necessarily changes the brain structurally and functionally. These changes can be further manipulated through non-invasive electrical brain stimulation. Studying these processes in the case of maths not only constitutes research of great practical impact – given the importance of numerical skills in today's society – but also makes use of maths as a suitable domain in which to study plasticity. In this thesis, I aimed to explore how expertise with numbers shapes brain and behaviour, and also the degree to which processing numbers is similar to other domains in terms of the necessity of healthy brain regions believed to underlie normal processing within and across these domains. In Study 1, behavioural and structural brain differences were found cross-sectionally between mathematicians and non-mathematicians. A double dissociation between those groups was found between grey matter density in the frontal lobe and behavioural performance: their correlation was positive for mathematicians but negative for controls. These effects may have been caused by years of experience, by congenital predispositions, or, plausibly, by both of these factors, whose disambiguation is non-trivial. Study 2 used transcranial random noise stimulation (tRNS) to assist arithmetic learning. A novel montage was used to enhance brain function during the stage when it is believed to be most involved. Real as compared to sham tRNS enhanced reaction times (RTs) and learning rate on a calculation-based task, but not on a retrieval-based task. The effects were only observed in conditions of high task difficulty. Study 3 examined structural MRI measures before and after arithmetic training to determine how either frontal or parietal tRNS applied with the task changes the structure of the brain longitudinally as compared to sham. Previous results (including those of Study 2) of behavioural facilitation in terms of enhanced RTs to calculation problems were replicated, and further interpreted. Both frontal and parietal tRNS modulated the changes that occurred, pre-to-post training, in terms of cortical volume and gyrification of frontal, parietal and temporal areas. Study 4 investigated the shared neural and cognitive resources used for processing numerical magnitude and musical pitch, by probing how stimulus-response compatibility (SRC) effects for each of the two dimensions compare in a group of mainly temporoparietal lesion patients with numerical impairments versus controls. A double dissociation was found in that numerically impaired patients did not show the number-based SRC effect but did show the pitch-based one, while control subjects demonstrated the opposite trend. Overall, the results of these studies leave us with three main messages. First, expertise in numbers and mathematics, whether acquired through years of experience (Study 1) or through a few days of tRNS-assisted training (Study 3), appears to be associated with complex changes in the morphology of several brain structures. Some – but not all – of these structures are maths-relevant, and, in the case of tRNS-assisted training, they are distal to the site of the stimulating electrodes. Second, tRNS can improve performance in arithmetic (Studies 2 and 3), although the mechanisms by which this occurs are not yet fully understood, neither neurally nor behaviourally. Third, I found (Study 4) that brain lesions leading to impairment in the number domain do not necessarily affect processing in other domains – such as pitch – that are otherwise linked to number via a putative common code in the parietal lobes.

While evidence suggests there is indeed a relationship between arterial stiffness and changes in brain structure and function cross-sectionally, the longitudinal relationship between arterial stiffness and changes in brain structure and function is unclear. Also unclear is whether a regional effect of arterial stiffness on brain structure exists, or if the effect is homogenous across brain regions. Using a healthy cohort of the UK Biobank study (N = 1858, meanSD: 61  7 years), we investigated the longitudinal association between changes in arterial stiffness index (ASI) and brain structure (grey matter cortical thickness, whole brain grey matter volume, white matter hyperintensity volume) and function (cognitive performance in 6 tests) over 2.5  1 years. We also examined the association between baseline ASI and all structural and functional brain outcomes 8-11 years post-baseline (N = 630). Prior to post-hoc correction, we observed a significant effect of changes in ASI over 2.5  1 years on grey matter cortical thickness in 11 brain regions contributing to reductions between 0.0004-0.0024mm annually, but none of the 11 regions remained significant post-correction. Following correction there was also no effect of changes in ASI on whole brain grey matter volume (p = 0.76), white matter hyperintensity volume (p = 0.84), or cognitive performance in the domains of interest. Baseline ASI was not associated with regional grey matter cortical thickness, white matter hyperintensity volume, or cognitive function, but did have a significant negative association with whole brain grey matter volume 8.5  1.05 (p = 0.015) years later and 11  1.02 (p = 0.03) years later. Our findings suggest that taken with the effect of age, elevations in ASI may have an additive effect to accelerate changes in brain structure beyond the range that is to be expected as a part of normal aging. Our findings also suggest the relationship between ASI and reductions in whole brain grey matter volume may require long-term exposure to elevations in arterial stiffness in otherwise healthy older adults. / Thesis / Master of Science in Kinesiology / Arterial stiffening both accompanies the normal aging process and can progress due to acquired health conditions. As arteries begin to stiffen the ability to buffer high pressure blood flow is impaired and can put microvasculature at risk of damage. Microvascular damage in the brain can disrupt blood and subsequent oxygen delivery to the brain. When delivery to the brain does not meet the metabolic demand, changes in brain structure brain can occur. Changes in brain structure are associated with impaired brain function, as well as potentially accelerating the progression of neurological diseases. What remains unclear is whether arterial stiffness impacts brain structure differently across regions or all regions homogenously. The purpose of this thesis was to examine the relationship between arterial stiffness and structural and functional changes in the brain over time (objective 1: 2-5 years; objective 2: 8-11 years). Our observations suggest that the progression of arterial stiffness had an effect that was equivalent to approximately 30% of the rate of grey matter tissue loss associated with normal healthy aging (~0.25% reduction in grey matter per year). We found no effect of changes in arterial stiffness on the progression of total grey matter volume, white matter lesions or brain function. We did observe a significant negative relationship between arterial stiffness at baseline and total grey matter volume 8-11 years later. We found no relationship between baseline arterial stiffness and brain structure or function 8–11-years post-baseline. Taken with the effects of normal aging, the loss of tissue in select brain regions associated with changes in arterial stiffness may result in grey matter reductions beyond the range associated with what is considered healthy or normal aging. The association of arterial stiffness and total grey matter volume 8-11 years later suggests that changes in whole brain structure are the product of long-term exposure to arterial stiffness.

Background: Children born very preterm are at an elevated risk of behavioural adjustment problems, particularly Attention-Deficit/Hyperactivity Disorder (ADHD) or inattention/hyperactivity difficulties. Importantly, these risks remain even after controlling for the effects of social risk factors correlated with very preterm birth. Behavioural outcomes in follow-up studies of children born very preterm are typically assessed using parent reports only. However, the extent to which behavioural problems are evident across multiple contexts (i.e., parent or teacher report) is not well known. Furthermore, the neonatal neuropathology underlying these behavioural difficulties in this population remains poorly understood. Aims: Three research studies are undertaken primarily to examine: (1) the degree of agreement between parent and teacher reports of child behaviour adjustment, and the extent of situational (parent- or teacher-identified) and pervasive (parent- and teacher-identified) inattention/hyperactivity problems at ages 4, 6, and 9 years among children born very preterm and full-term; (2) to cross-validate the classification of children with situational and pervasive inattention/hyperactivity problems across the ages of 4 to 9, for a clinical diagnosis of ADHD at age 9 years; (3) to document risk of persistent ADHD symptoms between ages 4 and 9 years in children born very preterm, and to examine associations between qualitative measures of neonatal cerebral white matter injury/abnormality and quantitative volumetric measures of cerebral structural development, identified using magnetic resonance imaging (MRI) at term equivalent age, and children’s later risks of persistent symptoms. Persistent ADHD symptoms were defined as behavioural inattention/hyperactivity problems shown at ages 4, 6, and 9, along with meeting the criteria for an ADHD clinical diagnosis at age 9 years. Methods: As part of a prospective longitudinal study, a regional cohort of 110 very preterm (≤ 33 weeks of gestation) and 113 full-term children born between 1998 and 2000 were studied from birth to age 9 years. At term equivalent age, all children born very preterm and 10 children born full-term underwent an MRI scan that was analysed using qualitative measures for cerebral white matter injury/abnormality, and quantitative volumetric techniques with tissue segmentation and regional parcellation for cortical and subcortical grey matter, myelinated and unmyelinated white matter, and cerebrospinal fluid. At ages 4, 6 (corrected for the extent of prematurity), and 9 years (uncorrected), children were screened for behavioural adjustment problems including inattention/hyperactivity symptoms using the parent and teacher rated Strengths and Difficulties Questionnaire (SDQ). At age 9, the Development and Well-Being Assessment (DAWBA) structured psychiatric interview was also completed with primary caregiver and an independent clinical diagnosis of ADHD determined by a child psychiatrist blinded to child’s perinatal history and group status. Results: Agreement between parent and teacher reports regarding child behaviour adjustment was lower for children born very preterm than full-term (mean alternative chance-correlated coefficient, AC₁ = 0.63 vs. 0.80). Across all assessment time-points, very preterm birth was associated with on average a 2-fold increased risk of behavioural inattention/hyperactivity problems. These elevated risks largely reflected high rates of situational symptoms (very preterm = 22.3% − 31.7%; full-term = 10.9% − 16.7%). In contrast, rates of pervasive symptoms were relatively modest (very preterm = 6.8% − 11.5%; full-term = 4.7% − 7.3%). Examination of the predictive validity of inattention/hyperactivity problems identified using parent and teacher reports showed that children exhibiting situational symptoms at ages 4 and 6 were much less likely than those exhibiting pervasive symptoms, for a subsequent clinical diagnosis of ADHD at age 9 years (very preterm = 29% − 47.8% vs. 66.7% − 75%; full-term = 13.3% − 22.2% vs. 33.3% − 40%). Furthermore, receiver operating characteristic curves fitted to the data showed that children born very preterm exhibiting inattention/hyperactivity problems at two or three time-points (area under curve, AUC = .909) have better predictive validity for later ADHD diagnosis, compared to those exhibiting symptoms at age 4 (AUC = .794) or 6 years (AUC = .813) only. Children born very preterm were also at an elevated risk of persistent ADHD symptoms across the ages of 4 to 9 years, with the risk being 5-fold higher than their full-term peers (13.1% vs. 2.8%). Results also revealed possible associations between neonatal neuropathology and later risk of persistent ADHD symptoms. There were no significant linear associations between increasing severity of qualitative neonatal MRI measures of white matter injury/abnormality and very preterm children’s later risk of persistent ADHD symptoms. However, reduction in total cerebral tissue volumes and corresponding increase of cerebrospinal fluid (adjusted for intracranial volume) were significantly associated with increased risk of persistent symptoms in children born very preterm (p = .001). In terms of regional tissue volumes, total cerebral tissues in the dorsal prefrontal region showed the largest volumetric reductions among all the subregions in children born very preterm exhibiting persistent ADHD symptoms, with 3.2 ml (7%) and 8.2 ml (16%) lower tissue volumes than children born very preterm and full-term without persistent symptoms, respectively. Conclusions: Reliance on a single informant to examine child behaviour outcomes at a single time-point may lead to an under- or over-estimation of later ADHD risks. Combining reports from multiple informants and repeated assessments over time may provide better clinical prognostic validity. Children born very preterm are at an increased risk of behavioural inattention/hyperactivity problems during their early school years; although risks of more severe, pervasive problems are relatively modest compared with situational problems. Behavioural adjustment difficulties recognised as early as during preschool age using standardised behaviour screening tools can be a reliable indicator for identifying children born very preterm at risk of subsequent ADHD diagnosis. Finally, study findings suggest that increased risk of ADHD symptoms in children born very preterm can at least in part be accounted for by disturbances to neonatal cerebral growth and maturation.

Einleitung: Risiken für Honigbienen stellen heutzutage schwindende natürliche Flächen und der Einsatz von Pestiziden in der Landwirtschaft dar. Flupyradifuron ist der Wirkstoff eines neuen Pflanzenschutzmittels der Bayer AG, das unter dem Namen „Sivanto“ vermarktet wird. Flupyradifuron an den nikotinischen Acetylcholin-Rezeptor im Gehirn der Honigbiene. Zielstellung: Ziel dieser Arbeit ist es, subletale Effekte von Flupyradifuron auf Verhalten und Gehirnstrukturen der Honigbiene zu untersuchen. Material und Methoden: Der Effekt einer chronischen Flupyradifuron-Applikation in unterschiedlichen Konzentrationen über zehn Tage auf die Mortalität, wurde in frisch geschlüpften Sommerbienen und langlebigen Winterbienen untersucht (N = 30 pro Behandlung, jeweils vier Replikate). Die statistische Auswertung erfolgte mit der Kaplan-Meier-Methode mit log-Rank Test. Nachdem Flupyradifuron einmalig an Honigbienen (N = 46, 47, 48 bzw. 55 pro Behandlung bei Nektar-sammelnden; N = 54, 68, 56 bzw. 62 pro Behandlung bei Pollen-sammelnden Bienen) verfüttert wurde, wurde deren Geschmackswahrnehmung getestet Im Folgenden wurden die Bienen mittels klassischer olfaktorischer Konditionierung auf einen Duft konditioniert. Das Gedächtnis wurde am nächsten Tag getestet. Zur statistischen Auswertung wurde die logistische Regression mit Post-Hoc Least Significant Difference Test angewendet. Es wurde eine Videoanalyse durchgeführt, um den Einfluss von Flupyradifuron auf die motorischen Fähigkeiten von Sommer- und Winterbienen zu untersuchen. Dazu wurde Flupyradifuron einmalig (N = 19 pro Behandlung im Sommer; N = 17 bzw. 16 pro Behandlung im Winter) oder über 24 h (N = 15 pro Behandlung im Sommer; N = 18 pro Behandlung im Winter) verabreicht. Zum Vergleich wurde das Experiment mit dem Neonikotinoid Imidacloprid bei Winterbienen wiederholt (N = 17 bzw. 16 pro Behandlung bei einmaliger Gabe; N = 16 pro Behandlung bei 24 h Gabe). Die statistische Auswertung erfolgte mittels einer nicht-parametrischen Varianzanalyse (Kruskal-Wallis H Test) und dem Pearson Chi-Quadrat Test. Um die Effekte von Flupyradifuron auf das Sammelverhalten der Bienen zu untersuchen, wurde die RFID („radio frequency identification“) Technik angewandt. Frisch geschlüpfte Arbeiterinnen (N = 100) wurden in einem separaten Käfig im Bienenstock gehalten und mit Flupyradifuron behandelt. Nach sieben Tagen wurden die Bienen in die Kolonie entlassen und ihr Flugverhalten für 40 Tage verfolgt. Das Experiment wurde zweimal durchgeführt. Die Kaplan-Meier Methode mit log-Rank Test wurde angewandt um Sammelbeginn und -ende zwischen den Behandlungen zu vergleichen. Anzahl und Dauer der Sammelflüge zwischen den Behandlungsgruppen wurden mit dem Mann-Whitney-U-Test verglichen. Um den Einfluss von Flupyradifuron auf Gehirnstrukturen zu untersuchen, wurden die Bienen über zehn Tage oral mit Flupyradifuron behandelt. Gehirne (N =10 pro Behandlung) wurden präpariert, Schnitte von 5 µm wurden hergestellt und mit Hämatoxylin/Eosin (H/E) gefärbt. Bei allen Versuchen wurde ein Signifikanzniveau von P < 0,05 festgelegt. Ergebnisse: In einer mittleren Konzentration von 1,0 µg pro Biene pro Tag war die Mortalität von Sommer- und Winterbienen in drei bzw. zwei von vier Replikaten signifikant erhöht. Eine zehnfach höhere Konzentration führte zu 100 % Mortalität, eine zehnfach niedrigere Konzentration war subletal. Flupyradifuron reduzierte die Geschmackswahrnehmung und das appetitive Lernen. Dabei hatte nur die höchste verwendete Konzentration (8,3 *10 4 mol/l) einen signifikanten Einfluss, zwei zehnfach niedrigere Konzentrationen hatten keinen Effekt. Eine einmalige Flupyradifuron-Gabe störte das normale motorische Verhalten von Bienen und führte zu motorischen Ausfallerscheinungen. Dies war bei Winterbienen stärker ausgeprägt als bei Sommerbienen und wurde durch eine hohe Dosis (8.3 *10 4 mol/l) hervorgerufen. Nach einer chronischen Gabe über 24 h waren die Veränderungen weniger stark ausgeprägt. Imidacloprid führte nicht zu motorischen Ausfallerscheinungen. Insektizid-behandelte Bienen zeigten signifikant früheres Sammelverhalten. Dies galt für beide Replikate. Im zweiten Replikat zeigten die behandelten Bienen zudem mehr Sammelflüge und diese dauerten länger. Die Analyse von Gehirnstrukturen nach der Behandlung mit Flupyradifuron mit Hilfe von Lichtmikroskopier brachte keine Veränderungen zu Tage. Schlussfolgerungen: In hohen Konzentrationen beeinflusst das neue Insektizid Flupyradifuron Kognition und Motorik der Honigbiene in ähnlicher Weise wie die teilweise verbotenen Neonikotinoide. In niedrigeren Konzentrationen sind die Effekte weniger stark ausgeprägt. Zukünftige Studien sollten mögliche synergistische Effekte von Flupyradifuron in Kombination mit Pflanzenschutzmitteln, wie Fungiziden, aber auch in Kombination mit Parasiten und anderen Krankheitserregern untersuchen. / Introduction: Changing landscapes and pesticides resulting from intensified agriculture are two of the main threats for honeybees. Flupyradifurone is the active ingredient of a new pesticide released by Bayer AG under the name of “Sivanto”. It binds to the nicotinic acetylcholine receptor (nAchR) in the honeybee brain, similar to neonicotinoids. Aim: The aim of this study is to investigate effects of flupyradifurone on honeybee behavior und brain structure. Material and methods: The effect of a chronic application of flupyradifurone in different concentrations on mortality was studied in newly emerged summer bees and long lived winter bees (N = 30 per treatment, four replicates) over a period of ten days. Survival was analyzed using Kaplan-Meier –Method with log-rank Test. After feeding foraging honeybees (N = 46, 47, 48 respectively 55 per treatment in nectar foragers; N = 54, 68, 56 respectively 62 per treatment in pollen foragers) a single dose of flupyradifurone, gustatory responsiveness was quantified. Afterwards the bees were trained to an odor using classical olfactory conditioning. Memory was tested the next day. Statistical analysis was conducted using Logistic Regression. For post-hoc multiple comparisons we used the Least Significant Difference Test. Video analysis was conducted to test the effects of flupyradifurone on honeybee motor abilities in young summer bees and long lived winter bees. Flupyradifurone was administered once (N = 19 per treatment in summer; N = 17 respectively 16 per treatment in winter) or over the period of 24 h (N = 15 per treatment in summer; N = 18 per treatment in winter). For comparisons this experiment was repeated with the neonicotinoid imidacloprid (N = 17 respectively 16 per treatment for single administration; N = 16 per treatment for 24 h application). Non-parametric analysis of variance (Kruskal-Wallis H Test) and Pearson Chi-Square Test were applied to determine the effect of the insecticides on motor behavior between the different treatment groups. To test effects of flupyradifurone on honeybee foraging, RFID (radio frequency identification) technology was applied. Newly emerged worker bees (N = 100) were taken in a separated cage on top of the bee hive and treated with flupyradifurone. After one week the bees were released into the colony and their flight behavior was tracked for 40 days. The experiment was repeated twice. Kaplan-Meier-Method with log-rank Test was applied for comparing onset and end of foraging between the two treatment groups. Trips per active day and duration per trip between the different treatment groups were compared using Mann-Whitney U-Tests. Effects of flupyradifurone on honeybee brain structure were analyzed. Bees were treated with flupyradifurone for ten days. Brains (N = 10) were dissected and 5 µm sections were produced and stained with hematoxylin and eosin (H/E). For all experiments a significance level p < 0.05 was determined. Results: The mortality experiment revealed comparable results in newly emerged summer bees and long lived winter bees. The mortality of an intermediate concentration of approximately 1.0 µg flupyradifurone per bee per day was in three respectively two out of four replicates significantly increased. A tenfold higher concentration led to 100 % mortality, whereas a tenfold lower concentration was sublethal. Flupyradifurone reduced taste and appetitive learning performance in honeybees foraging for pollen and nectar. Only the highest concentration (8.3 *10 4 mol/l) had significant effects, whereas two tenfold lower concentrations had no effects. Flupyradifurone disturbed normal motor behavior and evoked motor disabilities after a single administration. The observed effects were stronger in long lived winter bees than in young summer bees. However, only a high dose (8.3 *10 4 mol/l) had these strong effects. After a continuous administration over 24 h the observed effects were less severe. Imidacloprid did not lead to motor disabilities. Pesticide-treated bees initiated foraging significantly earlier than control bees. This was true for both replicates. In the second replicate flupyradifurone treated bees furthermore showed more and longer foraging trips. Analyzing honeybee brains using light microscopy, no altered brain structures were observed after treating honeybees with flupyradifurone. Conclusion: High concentrations of flupyradifurone influence honeybee cognition and motor abilities in a similar way as the partly banned neonicotinoids. In lower concentrations, the observed effects are less severe. Future studies should examine possible synergistic effects of flupyradifurone between in combination with other pesticides, such as fungicides, but also in combination with parasites and other stressors, such as diseases.

No description available.