About: Molecular and cellular neuroscience  

How is molecular and cellular neuroscience of interest?

The School would like to increase the number of doctoral students interested in using molecular and cellular approaches for investigating cognition.

For example: Autism and Alzheimer’s Disease


Autism is a serious neurodevelopmental disorder with an estimated frequency of approximately 2–6 per 1000. Autistic individuals exhibit restricted, repetitive, and stereotyped patterns of behaviour, interests and activities, and they typically display severely impaired social interaction and communication. Onset is generally observed between one and three years of age, and early signs may include, e.g., failure to respond to verbal cues, avoidance of eye contact, and engagement in clearly asocial activities such as twirling or rocking. Language development is generally delayed. Although some autistic individuals are also diagnosed  with general cognitive delay or mental retardation, in many cases, the observed cognitive abnormalities are exclusively deficits in communication; thus, investigations into the neurobiology of autism enable us to answer interesting questions about the nature of emotional development and social learning.
There have been significant developments in our understanding of the genetics underlying these behavioural abnormalities in recent years, and it is clear that several genes implicated in autism-associated disorders are essential for normal synaptic transmission. Neurexins and neuroligins, for example, both associated with autism, are neuronal cell adhesion molecules that form a trans-synaptic complex. Neuroligins interact with the autism-associated Shank family of scaffolding proteins at the post-synapse, and it has been shown that aberrations in the expression levels of these proteins influence the maturation and function of glutamatergic synapses. Several other genes implicated in developmental disorders likewise affect glutamatergic synaptic transmission, and, not surprisingly, individuals with autism and related disorders have a significantly increased risk for acquiring seizure disorders in childhood.

Alzheimer’s Disease

Alzheimer’s Disease is a degenerative disorder which affects a  large population in the Western world. The main risk factor is age. It is associated with a loss of memory and intellectual capabilities.
In the recent years a number of animal models has been developed which mimic some features of this disease process. Mice with a mutated form of the amyloid protein, for instance, are characterized by the formation of amyloid plaques as is found in the brains of Alzheimer patients. These mice also show cognitive deficits. At present a number of mouse models for Alzheimer’s Disease are available for the scientific community.
These mouse models are excellent tools to study the molecular basis underlying this disease. While research on the degeneration of neurons has been in the focus of the community, it has now become evident that also glial cells, in particular microglia and astrocytes, are affected by this disease process. Astrocytes have been recognized to be important elements for synaptic transmission which underlies all brain functions. Indeed, the synaptic elements do not only consist of pre- and postsynaptic elements but also of the astrocyte enwrapment.  Microglial cells have been recognized to be the pathologic sensors in the brain responding by a process called activation to any pathologic event. It has become, however, evident that this activation is a heterogeneous response varying between different diseases and during the course of the pathology. It is, thus, a challenging goal to understand which role astrocytes and microglia play for the onset and development of Alzheimer’s Disease.

Contact persons regarding general research area “Molecular and cellular neuroscience”

This page last updated on: 07 July 2015

Autism: which cell types are affected?
Genetic developments have enabled us to develop the necessary tools for investigations into the cellular basis of these disorders, and we are currently using transgenic in vitro and in vivo models to examine the electrophysiological and behavioural effects of specific disease-causing genetic aberrations. Several questions are clearly relevant for broadening our understanding of autism-associated neurodevelopmental disorders. For example, which cell types are affected by these gene defects? And which brain regions are implicated? Do mutations influence both glutamatergic and GABAergic transmission? Are there specific developmental time windows in which disease-causing mutations have greater influence on synaptic transmission?

Photograph © Laura Viefhues