Servicio de Información Comunitario sobre Investigación y Desarrollo - CORDIS

Periodic Report Summary 1 - COGNITIONNET (Multilevel brain network analyses leading to improved therapeutics for cognitive impairments)

Cognitive abilities change with development and age. Cognitive development during childhood and adolescence depends on an intellectually challenging environment, but is robustly affected in various forms of mental retardation. Adult cognitive abilities are strongly correlated with a person’s success in life. Finally, cognitive decline is an important problem during aging and is accelerated in neurodegenerative disorders like Alzheimer’s disease. Lifetime cognitive wellbeing is of the utmost importance in a society where life expectancy and individual demand for socio-economic participation are increasing, and where the financial burden on health care needs to be contained. CognitionNet investigates brain mechanisms of cognition at the molecular, cellular, neural network and behavioural level, both from a basic and a clinical perspective and aims to integrate the results to develop novel treatment options for various forms of cognitive impairment.
Four scientific work packages (WPs) have been constructed, in which the individual projects are harboured, to build on the availability of existing databases in order to facilitate genetic approaches and combining mouse models and human cohorts for cross-species analysis with the following objectives:
WP1. The process of cognition is adaptable throughout life, in which one can learn new skills even at older age. In order to prevent early cognitive decline, a full exploitation of the extent of our natural cognitive plasticity is needed. This work package aims to discover plasticity of cognition during adulthood using attention and contextual memory as read-out systems. Individual projects focus on learning how molecules or cell types contribute to processes underlying cognition. Several tools have been created to enable creating causality for these molecules or cell types in cognitive control.
WP2. The level of cognitive control is set in the brain during early development, which is apparent in developmental neurological diseases related to autism spectrum disorder. Using mouse models and human patient material, the role of genes with human mutations related to these diseases are studied in the context of synaptic plasticity and cognitive control in adulthood. Individual projects focus on models or patient cell lines for developmental diseases caused by known and unknown genetic mutations, such as Rett syndrome, autism, and fragile X syndrome. Several tools have been created to dissect the role of specific molecules or cellular processes involved in neuronal communication.
WP3. Cognitive decline occurs in normal aging humans and is severely accelerated in patients with neurodegenerative diseases such as frontotemporal dementia (FTD) and Alzheimer's disease (AD). This work package aims to identify novel therapeutic entry points for treatment of age-related cognitive decline. Individual projects focus on models and patient cell lines of neurodegenerative diseases (Alzheimer’s, vanishing white matter), as well as on data from these patients. Tools and protocols have been optimized to dissect the role of specific cell populations in the disease as well as to find non-invasive biomarkers for disease.
WP4. Cognitive malfunctioning is a vital aspect of multiple psychiatric diseases that co-occur, such as attention and impulsivity or depression in people suffering from ADHD, but also being higher at risk for depression and addiction. Using single gene mutation studies and interference at the level of the synapse and the neuronal network in relation to cognitive behaviour, we aim to disentangle affected states of the network that lead to maladaptive behavioural output. Individual projects focus on characterizing the neuronal network and accompanying molecular mechanisms underlying comorbid features (e.g., addiction, depression, autism) that affect cognition. Several tools have been created to enable creating causality for these molecules or cell types in cognitive control.
Together, insight in the healthy and disease brain will provide new insight into basal (developmental) mechanisms of cognitive processing, and will assist in the development of novel treatment options for various forms of cognitive impairment.
Trainees have publicly presented their plans at an early stage, allowing them to actively participate in the scientific discussions and to gain insight in the strategic planning of their own research project. Furthermore, they received general introduction courses in complementary fields. For their personal effectiveness transferable skill courses have been followed, as well as Dutch language courses. The first secondments have been performed by several trainees, some in academia, and some at industrial partners. All of these have been received enthusiastically. Specific focus has been on broadening the career prospects of the trainees by providing inter-ITN training and dissemination with the INSENS network.
Trainees have performed poster presentations for the scientific community on several occasions (Dutch Neuroscience meeting, mid-term meeting with MSCA ITN INSENS, Graduate school Neuroscience meeting). In addition, trainees have participated in several dissemination events either for those possibly participating in academia (6-VWO students), as well as the general public; for example participation in the science weekend ‘weekend van de Wetenschap and evening ‘Avond van de Wetenschap’, generating a video clip about their scientific motivation and goals, and spending a day with terminal cancer patients.
Supervision arrangements have been made, in line with the graduate school Neuroscience and the VU University Amsterdam, including individual assignment to a mentor (experienced staff scientist not in direct relation to the supervisor), as well as appointment of the Ombudsperson, who is not related to the project.


Yvonne Kops, (Managing director FALW)
Tel.: +31 20 5987304
Fax: +31 20 5989950
Correo electrónico
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