New York (Sept. 21, 2008) A study in the Sept. 21 on-line edition of Nature Medicine describes the function and interaction of a critical molecule involved in cell death in Alzheimer's disease patients. These new findings reveal that blocking this molecule, called Cyclophilin D (CypD), and development of surrounding mitochondrial targets may be viable therapeutic strategies for the prevention and treatment of Alzheimer's disease, according to Shi Du Yan, Ph.D., professor of clinical pathology in the Department's of Pathology and Surgery and in the Taub Institute for Research on Alzheimer's Disease and the Aging Brain at Columbia University Medical Center, who led the multi-center research.
This paper strengthens the concept that mitochondrial permeability pores may be central in mitochondrial and neuronal malfunction relevant to Alzheimer disease. Dr. Yan and her colleagues offer new insights into the mechanism underlying amyloid beta (Aβ)-mediated mitochondrial stress through an interaction with CypD, which is linked to synaptic plasticity and learning/memory. Importantly, these findings may help explain the mechanism of action of a medication already in use in clinical trials.
Mitochondria, the microscopic parts found outside the nucleus of the cell that produce a cell's energy, are central players in mediating neuronal stress relevant to the pathogenesis or development of neurodegenerative diseases such as Alzheimer's disease. Mitochondrial dysfunction, or a problem with the cellular exchange of energy, is an early event observed in Alzheimer's disease. Recent studies have provided substantial evidence that mitochondria serve as direct targets for amyloid beta (Aβ) protein mediated neuronal toxicity. The observations that Aβ progressively accumulates in cortical mitochondria from Alzheimer's disease patients and in brains from transgenic Alzheimer's disease type mouse models suggest the role of mitochondrial Aβ i
|Contact: Karin Eskenazi|
Columbia University Medical Center