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Fortschr Neurol Psychiatr. 2009 Aug;77 Suppl 1:S21-4. doi: 10.1055/s-0028-1109601. Epub 2009 Aug 14.

[The role of blood-brain barrier in the pathogenesis of Alzheimer dementia--implications for immunological therapies for plaque dissolution].

[Article in German]

Author information

1
Universität Rostock, Klinik und Poliklinik für Neurologie, Neurodegeneration Research Lab, Gehlsheimer Strasse 20, Rostock. jens.pahnke@med.uni-rostock.de

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder affecting more than 27 million people worldwide and leading to severe social-economic problems. One characteristic hallmark of AD--the amyloid plaques--are still being discussed to be one important triggering factor. However, current animal and autopsy studies refer to soluble and highly toxic A block oligomers as the deadly agent for the neurons. Current therapies mainly rely on the abatement of symptoms without antagonizing the etiology of the disease. Potential new approaches address reduced production, increased degradation and/or evacuation of toxic A block peptides from the brain. Among others one important group of target-proteins are the ABC transporters of the blood-brain barrier which contribute importantly to the detoxification of the brain. Changes of specific transport functions evoke important alterations for the known pathogenesis and future therapies of AD, especially approaches that target plaque dissolution and plaque reduction.

PMID:
19685385
DOI:
10.1055/s-0028-1109601
[Indexed for MEDLINE]

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