Amyloid- β May Cause Mitochondrial Dysfunction in Alzheimer ' s Disease

This study reinforces the toxicity of oligomeric amyloid-β on neuronal mitochondria and stresses the importance for protective compounds to protect the mitochondria from oligomeric amyloid-β toxicity." In the new study, cells known as pyramidal neurons, extracted from the hippocampus of patients who died of Alzheimer's, display a marked reduction in the expression of a suite of mitochondrial genes, pointing to their degradation by OAβ. The reduction of mitochondrial gene expression was also seen when cells belonging to a human neuroblastoma cell line were exposed to OAβ. The authors stress that not all types of nervous system cells are implicated in the mitochondrial dysfunction brought on by exposure to OAβ. Hippocampal astrocyte and microglia cells taken from the same AD-afflicted brains did not display reduced mitochondrial function. One problem with the amyloid theory of Alzheimer's disease is its inconsistency. Researchers have reported that some elderly patients, bearing heavy burdens of amyloid plaque in their brains, lack any measurable cognitive deficit, while other patients showing little to no amyloid buildup nevertheless display severe Alzheimer's-like dementia. These facts have led researchers to seek other processes occurring at the earliest stages, which may kick the disease into gear. One of the most promising avenues of new research is the mitochondrial cascade hypothesis, which places these energy-delivering powerhouses of the cell at the ...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs