The senile plaque that derives from β amyloid peptide and neurofibrillary tangles are implicated as the causes for the degeneration of neurons in Alzheimer’s disease. However, the cerebellum suffers extensive cell death during late stages of the disease even though it is relatively free of neurofibrillary tangles. This suggests the possibility that the neurotoxicity from the β amyloid may provide the main source of degeneration. These authors examined that question, and find evidence that specific oligomers of the β amyloid promote massive calcium overload of mitochondria, which might be responsible for cell death. They also found that non-steroidal anti-inflammatory drugs such as salicylate and ibuprofen inhibit mitochondrial calcium overload, which may point to new treatments for preventing this damage.
