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Last update:
24.08.2010

Neurotalks

Lectures and seminars in Goettingen for researchers in the field of neuroscience.
As a service for the neuroscience community the CSN maintains a website containing announcements for all neuroscience talks in Goettingen that we are aware of. Should you like to add an entry, please send announcements of your upcoming event to the webmaster.

CSN Plenary meeting

10.11.2010		17.15 Uhr
18.11.2009		18.15 Uhr
17.12.2008		17.15 Uhr

CSN Board meetings

Date		Time
22.09.2010		18.15 Uhr*
06.10.2010		18.15 Uhr*
10.11.2010		18.15 Uhr*
08.12.2010		18.15 Uhr*
*vorbehaltlich - bei neuen Vorstellungsgesprächen Vorverlegung

Past Events

• 2009 CSN Lecture 2009 CSN Lecture

  Proteolysis in Alzheimer's disease: Metabolism of amyloid beta peptide and involvement of the calpain-calpastatin system

  Prof. Dr. Takaomi Saido
  RIKEN Brain Institute, Japan

  Alzheimer's disease (AD), a predominant cause of dementia, stands out as a major threat against our present and future wellbeing. AD can be divided into two categories: Familial AD (FAD) and Sporadic AD (SAD). All the known FAD cases are dominantly inherited. Phenotypic analyses of the FAD mutations have identified amyloid ß peptide (Aß) as a primary pathogenic agent, although FAD is out-numbered by SAD, for which aging is a major risk factor. SAD accounts for more than 90% of all AD cases.

  The conversion of what has been interpreted as "normal brain aging" to SAD via a transition state, i.e. mild cognitive impairment (MCI), appears to be a continuous process caused primarily by aging-dependent accumulation of amyloid ß peptide (Aß) in the brain. This notion give us a hope that, by manipulating the brain Aß levels, we may be able not only to prevent and cure the disease but also to partially control some very significant aspects of brain aging.

  Aß is constantly produced from its precursor and immediately catabolized under normal conditions, whereas dysmetabolism of Aß seems to lead to pathological deposition upon aging. We have focused our attention on elucidation of the unresolved mechanism of Aß catabolism in the brain and discovered that a neutral endopeptidase, neprilysin, regulates the steady-state levels of Aß. Because there is inverse relationship between neprilysin expression and Ab quantity and because neprilysin expression/activity declines upon aging, the aging-dependent neprilysin down-regulation is likely to be one of the causal factors for the disorder. In turn, Aß burdens in aging brains can be reduced by up-regulating the catabolic mechanism involving neprilysin, which can degrade both monomeric and oligomeric forms of Aß.

  We also discovered that a particular Ab species accumulates in AD brain: Ab that starts with pyroglutamate (pE) at position 3, Aß3(pE)-42. Aß3(pE)-42 is more prone to oligomerize and more resistant to in vivo degradation. We show that neprilysin is involved in generation of Aß3(pE)-42 as well.

  We are also interested in the molecular neuropathology downstream of Ab deposition, which is likely to involve perturbation of calcium homeostasis. We thus have investigated a possible role of calpain, calcium-activated neutral protease. The calpain-calpastatin system appears to influence Ab amyloidosis, tau phosphorylation, microgliosis and somato-sendritic dystrophy, suggesting that calpain can be another pharmacological target for prevention and treatment of AD.

• 2009 CSN Minisymposia

• 2004/2005

• 2003/2004

  
  

Past Board Meetings

18.08.2010		18.15 Uhr
28.07.2010		17.45 Uhr
09.06.2010		17.15 Uhr
12.05.2010		16.45 Uhr
07.04.2010		17.45 Uhr
10.02.2010		18.15 Uhr
14.10.2009		18.15 Uhr
02.09.2009		17.00 Uhr
24.06.2009		17.00 Uhr
03.06.2009		17.00 Uhr
29.04.2009		17.15 Uhr
04.03.2009		18.15 Uhr
07.01.2009		18.15 Uhr
03.12.2008		18.15 Uhr
05.11.2008		17.15 Uhr
15.10.2008		18.15 Uhr
24.09.2008		18.15 Uhr
14.07.2008		17.30 Uhr