Gastgeber: Abteilung Neurologie Ort: Max-Planck-Institut für Kognitions- und Neurowissenschaften

Dr. Felix Hasler | Why depression is not just like diabetes. Promises and disappointments of biological psychiatry

Cognitive Neurology Lecture

Prof. Hartwig Siebner | Causal brain mapping: How gets the brain a handle on its actions?

Gastvortrag

Prof. Thomas Hummel | Does it matter when the sense of smell is lost?

Gastvortrag

Dr. Lorenzo Stafford | Smelling, eating and eating! A journey through our oldest sense and its link to a very modern epidemic

Cognitive Neurology Lecture

Sarah Garfinkel | The dynamic relationship between body, brain and negative emotion

Cognitive Neurology Lecture

Tom Fritz | From empirical music research to intervention in therapy

Institutskolloquium: Institutskolloquium (intern)

Sebastian Halder, PhD | Increasing accuracy and speed of BCI paradigms and applications

Gastvortrag
Brain-computer interfaces (BCIs) provide a non-muscular communication channel for patients with latestage motoneuron disease (e.g., amyotrophic lateral sclerosis (ALS)) or otherwise motor impaired people. Unfortunately, about a third of the potential users of BCIs are unable to use these systems with sufficient accuracy. Particularly worrisome, this number increases with the degree of impairment of the users. Thus, it is important to (1) develop new methods and BCI paradigms to increase accuracy, (2) determine possible causes for a lack of aptitude and (3) ensure that BCI applications have minimized complexity. In this talk novel auditory BCI paradigms and BCI applications that address these issues will be presented and possible approaches for the further development of communication methods for completely paralysed users discussed. [mehr]

Dr. Vadim Nikulin | Multimodal investigation of spatio-temporal brain dynamics: neuroscientific and clinical perspectives

Gastvortrag

Dr. Stefan Haufe | What can non-invasive neurophysiology tell us about brain connectivity?

Gastvortrag

Dr. Elinor Tzvi-Minker | Motor learning and the diseased brain: what can we learn from patients with cerebellar ataxia?

Gastvortrag

Dr. Christian Benedict | Energy balance out of balance following sleep loss

Gastvortrag

Maria Nazarova, PhD | Multimodal assessment of the motor system in normal subjects and stroke patients

Gastvortrag

Elena Azañon Gracia | Remapping touch from skin to space

Gastvortrag

Prof. Shu-Chen Li | Neurocognitive aging of the frontal-striatal-hippocampal circuitry: Implications for memory, spatial learning and goal-directed behavior in old age

Gastvortrag
The efficacy of various neurotransmitter systems declines with advancing age. Of particular interest, various pre- and post-synaptic components of the frontal and striatal dopaminergic systems show substantial negative age-related differences across the adult life span. Furthermore, anatomical and functional changes in the frontal and hippocampal regions are also hallmarks of brain aging. This talk will selectively highlight findings from recent neuroimaging, pharmacological and genetic studies about aging of the frontal-hippocampal-striatal circuitry and the implications for memory, spatial learning, and sequential decision-making in old age. [mehr]
Understanding changes in cerebral and cerebellar motor representation during long-term motor training might help to develop most effective training procedures. For brain damage after stroke, these neuroplastic processes are different than those observed in healthy volunteers. Several factors modify training progress and motor representation in these patients. This talk will summarize recent findings on these issues and will focus predominantly on upper limb motor training. [mehr]

Dr Patrick Freund | Tracking diaschisis across the neuroaxis: insights from neuroimaging

Kognitive-Neurologie-Vortrag
Recovery from spinal cord injury – and its attendant neurodegenerative processes – can follow a complicated trajectory spanning several years after trauma, where the ensuing diaschisis (meaning "shocked throughout") affects the entire neuroaxis. With potential treatments targeting repair of the injured spinal cord, there is an imperative to improve clinical trial design and efficiency, optimise patient stratification in the context of disease heterogeneity and identify potential trial outcome measures. The ability to track trauma-induced structural changes across the neuroaxis provides the opportunity to quantify pathological processes driving diaschisis and recovery-related plasticity. During my talk I will present evidence of progressive volume and microstructural changes (myelin and iron content) following acute spinal cord injury using state-of-the-art computational anatomy and post-processing tools. Further I will show latest developments of high-resolution MRI sequences and optimized post-processing methods to assess at the voxel level spinal cord grey and white matter changes. Finally, I will outline an integrative framework, which attempts to identify subgroups of neurologic disorders beyond standard clinical phenotyping – and to improve functional outcome with individualized treatment (i.e., precision neurology). This framework, franchised under the term “Embodied Neurology”, pays special emphasis on the reciprocal information flow between the body, spinal cord and brain. Spinal cord injury is a particularly interesting model in the context of EN as a focal traumatic lesion in the spinal cord has far reaching consequences in terms of both cortical reorganization at distant sites (cf. functional diaschisis) and the functional architecture within and beyond the spinal cord (cf. structural diaschisis). To establish EN there is a pressing need for further developments in neuroimaging with the aim to unify structural and functional biophysical models in order to link pathology to phenomenology with greater precision. [mehr]

Prof. Shu-Chen Li | Neurocognitive aging of the frontal-striatal-hippocampal circuitry: Implications for memory, spatial learning and goal-directed behavior in old age

Gastvortrag
The efficacy of various neurotransmitter systems declines with advancing age. Of particular interest, various pre- and post-synaptic components of the frontal and striatal dopaminergic systems show substantial negative age-related differences across the adult life span. Furthermore, anatomical and functional changes in the frontal and hippocampal regions are also hallmarks of brain aging. This talk will selectively highlight findings from recent neuroimaging, pharmacological and genetic studies about aging of the frontal-hippocampal-striatal circuitry and the implications for memory, spatial learning, and sequential decision-making in old age. [mehr]

Prof. Thomas Klockgether | Clinical and biological characteristics of ataxia disorders

Gastvortrag
In Clinical Neurology, ataxia denotes a syndrome of motor incoordination that typically results from dysfunction of the cerebellum and its afferent and efferent connections. Ataxia is also used to denote a group of neurodegenerative diseases of the cerebellum and its connections that are clinically characterized by progressive motor incoordination. Many of the ataxias have genetic causes, but there are also sporadic degenerative ataxias and ataxias which are due to acquired non-genetic causes. Overall, there is an enormous degree of heterogeneity among the ataxias with an estimated number of more than 150 different, molecularly defined diseases. Our research is focusing on the common, autosomal dominantly inherited spinocerebellar ataxias (SCA) which are caused by translated CAG repeat expansion mutations that code for an elongated polyglutamine tract within the respective proteins. To define the phenotype and natural history of these disorders we recruited a cohort of more than 500 patients and followed them over more than 8 years. Multivariate models allowed to explain up to 60% of the variability of the ataxia severity at baseline. Modelling of disease progression revealed genotype-specific patterns and identified biological factors that determine the rate of progression. MRI studies showed progressive grey and white matter tissue loss in cerebellum, brainstem and basal ganglia. Studies of a cohort of more than 300 apparently healthy SCA mutation carriers showed that first signs of impaired coordination and tissue loss of the brainstem or cerebellum occur more than 10 years before the clinical onset of ataxia. These observation led to a refined disease model of ataxia disorders that considers ataxia as a late disease stage which is preceded by extended asymptomatic and preclinical disease stages that offer a time window for early therapeutic intervention. Although CAG repeat expansion mutations are now known for more than two decades the mechanism how these mutations cause neurodegeneration remain far from clear. There is one component which is due to the toxic properties of proteins or protein fragments that contain elongated polyglutamine tracts. However, there are additional components that depend on the protein context of the polyglutamine tract and are disease specific. Currently, there is no treatment for SCA. Experimental work in cells and animals aims to reduce levels of mutant proteins using RNA interference (RNAi)and antisense oligonucleotides (AONs). An alternative approach is protein modification through AON-mediated exon skipping. As there are many obstacles to translate these approaches into clinical application there is renewed interest in finding drugs that interfere with cerebellar neuronal activity and thereby symptomatically improve ataxia. [mehr]

Dr Adrian Fischer | Dissociating reward- and information-based learning using EEG and fMRI

Gastvortrag
Human decision making often involves weighting of values obtained via the rewarding quality of experience, but can uniquely incorporate more abstract aspects such as information about possible long-term consequences. While the former is computationally simple and efficient, the latter requires utilization of a model about the world. I will present results of two studies aiming to disentangle unique learning mechanisms for both propensities. The first will focus on the cortical temporal dynamics of learning from reward compared to information revealed in the human EEG. The second will focus on regional specificity of neural correlates of learning from model-free and model-based outcomes that dissociate ventral from dorsal striatum in the fMRI. [mehr]

Yasser Iturria Medina, PhD | Multifactorial modeling of neurodegenerative progression

Kognitive-Neurologie-Vortrag

PhD Hadas Okon-Singer | Factors modulating emotional reactions: Attention, personality and neural architecture

Kognitive-Neurologie-Vortrag

Lieneke Janssen | Breaking bad habits – A meditation on the neurocognitive mechanisms of compulsive behaviour

Gastvortrag
We all have our habits, good and bad. But only for some, habits go from bad to worse and behaviour becomes compulsive, as we see for example in addiction or clinical overeating. How is it that a useful mechanism such as our habit system can come to work against us? Why does it happen for only some and not others when faced with tempting rewards? And how can we get back in control? In my doctoral studies I aimed to increase our understanding of this by investigating the neural and cognitive mechanisms underlying compulsive gambling (in gambling addiction) and eating behaviour (in a non-clinical population). Building on an extensive body of addiction literature, I used a variety of experimental paradigms to tap into different aspects of compulsive behaviour. I focussed in particular on altered reward processing and loss of control over automatic tendencies triggered by reward-related stimuli. Furthermore, I investigated the effects of a pharmacological (dopamine) and a behavioural (mindfulness) intervention on reward processing. [mehr]
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