Psychische Erkrankungen in der Lebensspanne ... - DGPPN

Topic 4 G Affektive Störungen, F3 // Affective disorders, F3
of alterations in glutamatergic neurotransmission and disturbances
in cerebral glucose utilization in affective disorders (tripartite synapse,
energy-dependent glutamate recycling, involvement of
S100B+ astrocytes).
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Glial Pathology in Mood Disorders – Pathomechanisms
Matthias Rothermundt (Universitätsklinikum Münster, Psychiatrie
und Psychotherapie)
Introduction: In major depression a reduction of glial cells and a
change in the activation status of astrocytes has been shown recently.
This presentation focuses on the potential impact of these
alterations for the pathogenesis of depressive disorders.
Method: Various pathomechanisms relevant for the development
of major depression are assessed with respect to the involvement of
glial cells.
Discussion / Results: Increased levels of inflammatory mediators
as demonstrated in major depression induce microglial activation
interfering with excitatory amino acid metabolism. The loss of astroglia
disturbs the balance of anti- and pro-inflammatory substances
and further impairs the removal of excitatory amino acids.
This ultimately leads to a disruption of the balance between neuroprotective
and neurotoxic factors what might eventually lead to depression.
In addition, a change in astrocyte function also interferes
with the kynurenine pathway resulting in an excess of quinolinic
acid which is considered neurotoxic. Furthermore, the kynurenine
pathway is closely linked to serotonin which is regarded as a pertinent
transmitter for depression, and to the inflammatory system.
There is increasing evidence that glial dysfunction might be involved
in the pathogenesis of depression.
004
Glial Pathology in Mood Disorders – fMRI and MR Spectroscopy In
vivo.
Martin Walter (Otto-von-Guericke-Universtität, Klinik für Psychiatrie,
Magdeburg)
Introduction: Recent imaging studies in major depressive disorder
have pointed out regionally specific disturbances in brain function,
with spatial and functional specificity that exceedes most histological
post mortem studies, which normally focus on parts of brain
specimen. The latter methods however provide a more direct insight
in impaired cellular and molecular systems, that normally remains
invisible to non invasive MR methods.
Method: Multimodal MR studies using task based functional and
resting state MRI and molecular profiling as done with MR spectroscopy
is proposed to link observables from both approaches and
combine evidences from histological and MR studies.
Discussion / Results: It will be shown how combined MRS-fMRI
studies are usefull in providing a new integrative framework for
molecular hypothesis testing and how specific transmitter systems
may be involved in commonly observed deviant (brain) functions
in MDD.
005
Glial Pathology in Schizophrenia – Degenerative or Adaptive Processes?
Peter Falkai (Universitätsklinikum Göttingen, Psychiatrie und Psychotherapie)
Patients with schizophrenia reveal in vivo and post mortem studies
typical pattern of subcortical atrophy with a focus in frontal-temporal
regions including the hippocampus. In a systematic stereological
investigation of the posterior hippocampus no change in the
numbers of macroneurons, interneurons and astroglia were found.
However, the circumscribed reduction of oligodendroglia in the
CA4-region was detected. This is in accordance with the published
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literature demonstrating, that schizophrenia is not a classical neurodegenerative
process showing an increase of astroglia. There is
however some evidence for a subtle increase in microglia which is
however unspecific and can be due to several adverse events. A circumscribed
reduction of oligodendroglia would well fit to the hypothesis
of reduced neuroregenerative capacities in schizophrenia
leading to a functional neuronal network. Reference: Schmitt A,
Steyskal C, Bernstein HG, Schneider-Axmann T, Parlapani E, Schaeffer
EL, Gattaz WF, Bogerts B, Schmitz C, Falkai P (2009). Stereologic
investigation of the posterior part of the hippocampus in schizophrenia.
Acta Neuropathol 117(4): 395-407
Freitag, 27. 11. 2009, 15.30 – 17.00 Uhr, Saal VIP 2
S-116 Symposium
Bedeutung von Früherkennung und Frühintervention für den
Krankheitsverlauf Bipolarer Störungen (Symposium mit der
Deutschen Gesellschaft für Bipolare Störungen e. V.)
Vorsitz: M. Bauer (Dresden), G. Juckel (Bochum)
001
5 Jahre Psychosen Ersterkennungs- und Behandlungsprojekt (PEB):
Was haben wir gelernt?
Martin Lambert (UKE Hamburg-Eppendorf, AB Psychosen)
002
Symptomatische Phasen in der Entwicklung bipolarer Störungen
– Gibt es mehr als ein Prodrom?
Andrea Pfennig (Uniklinikum Dresden, Klinik für Psychiatrie)
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Hirnmorphologische Veränderungen vor manischen Ersterkrankungen
Andreas Bechdolf (Uniklinik Köln, Klinik für Psychiatrie)
S. Wood, C. Pantelis, P. D. McGorry
Introduction: There is now numerous reports of neuroanatomical
abnormalities in people with bipolar disorder. However, it remains
unclear whether those abnormalities predate the onset of bipolar
disorder.
Objective: To determine whether neuroanatomical abnormalities
in key brain regions predate the onset bipolar disorder. Design:
Cross-sectional magnetic resonance imaging study prior to the
onset of bipolar disorder and prior to the prescription of mood stabilizers
or antipsychotics.
Methods: Youth-focussed psychiatric service and university medical
setting. Participants: 11 young people clinically at ultra highrisk
of development of psychosis (UHR), who all developed bi -
polar I or II disorder at follow-up (median time to onset 328 days
– UHR-BP), 11 matched UHR participants, who had no psychiatric
diagnosis after at least 12 months follow-up (UHR-Well) and
11 matched healthy controls (HC).
Discussion / Results: Amygdala, hippocampus, insula, lateral ventricular
and whole brain volumes. Results: Amygdala and insula
volume reductions were more pronounced in the UHR-BP than in
the UHR-well and HC group. Lateral ventricle, whole-brain and
hippocampal volumes did not differ between groups. Conclusions:
If these findings are confirmed, they suggest that imaging investigations
could help to distinguish people who will subsequently
de velop fisrt episode mania from those who will not, at least in
symptomatically en riched samples.