Die aktuelle Orientierungshilfe in 5 Bänden - Vlaamse Vereniging ...

DGPPN Congress 2009 – English Programme
Plenary Lectures
Judith L. Rapoport
Pierluigi Nicotera
100
Thu, 26. 11. 2009 // 12.15 – 13.15 h
Brain development and childhood psychopathology
Chair: Peter Falkai (Göttingen, Germany)
Speaker: Judith L. Rapoport (Bethesda, USA)
ErD
Many if not most psychiatric disorders have now been hypothesized to be in part due to
abnormalities in brain development. The stability of the NIMH intramural research program
permits long­term brain imaging studies to establish norms, and relate abnormalities to diagnosis
and clinical outcome.
Over the past 20 years we have carried out a prospective longitudinal anatomic brain MRI
study of children and adolescents with Attention Deficit Hyperactivity Disorder (ADHD),
Childhood Onset Schizophrenia (COS) and healthy controls (including monozygotic and
dyzygotic twin pairs) who returned for scans every two years across a 10 year period. The
patients were followed clinically and took part in various treatment trials. In addition DNA
was obtained from all subjects.
The normative data indicates the non­ linearity of cortical brain development and marked
sex differences in timing of developmental trajectories. Twin data indicates that heritability
varies by brain region and by developmental period. For example the cerebellum appears
relative less heritable and is the last structure to reach adult volume. There is a “back to
front wave” of development of cortical thickness; delayed frontal development is associated
with superior IQ.
Finally, brain developmental trajectories have strong and diagnostically specific patterns for
clinical disorders. For example, cortical development in COS is marked by an accelerated
rate of cortical “pruning” during adolescence. For ADHD there is a delay in the rate of frontal
cortical maturation (marked as age of peak cortical brain thickness), which may be associated
with good outcome. Similarly, the devel opmental trajectory for a parietal region in the
“posterior attentional system” is also associated with good outcome. Thus trajectories may
identify genetic and clinical outcome groups and be useful intermediate phenotypes.
Fri, 27. 11. 2009 // 12.15 – 13.15 h
Synaptic degeneration and plasticity in neuro degenerative
diseases
Chair: Wolfgang Maier (Bonn, Germany)
Speaker: Pierluigi Nicotera (Bonn, Germany)
ErD
In recent years, it has become clear that cells can execute not only one, but several death
programs, especially under pathological conditions. The predominance of one or another
death executing mechanism may be dictated by factors as different as energy requirement,
signalling molecules and the intensity of a given insult. In addition, differentiation patterns
may direct tissue­specific death routines. This is particularly true of neurons, where spatial
selectivity of death signals and promiscuity of execution systems can result in the complex
and relatively slow demise, which occurs in neurodegenerative disease. For example, selective
synaptic damage is sufficient to trigger distinct executions for axo­dendritic networks
and cell bodies in central neurons.
In addition, because the machineries for cell death execution seem to be expressed constitutively
in virtually all cells, their conservation from unicellular to multicellular organisms
may be due not to their death­related role, but rather to their possible survival functions. In
this case, loss of function of pro­death molecules may have harmful consequences. I shall
describe mechanism involved in synaptic proning and plasticity and their relationship to
neurodegenerative disorders.