Our knowledge of Alzheimer’s disease has grown rapidly in the past few decades but it has proven difficult to translate fundamental discoveries about the disease into new treatments. Now researchers have developed a model of the early stages of Alzheimer’s disease in rhesus macaques. The macaque model could allow better testing of new treatments.
The model was developed by Professor John Morrison’s laboratory at the CNPRC, in collaboration with Professor Jeffrey Kordower of Rush University Medical Center and Paramita Chakrabarty, assistant professor at the University of Florida.
Alzheimer’s disease is thought to be caused by misfolding of the tau and amyloid proteins. Misfolded proteins spread through the brain, leading to inflammation and cell death. Tau protein is commonly found in neurons of the brain and central nervous system, but not elsewhere.
Researchers think that decades may elapse between the silent beginnings of the disease and the first signs of cognitive decline. Understanding what happens over these years could be key to preventing or reversing symptoms of Alzheimer’s disease. But it is difficult to study therapeutic strategies without a powerful animal model that resembles the human condition as closely as possible, Morrison said. Much research has focused on transgenic mice that express a human version of amyloid or tau proteins, but these studies have proven difficult to translate into new treatments.
New translational models needed
Humans and monkeys have two forms of the tau protein in their brains, but rodents only have one, said Danielle Beckman, postdoctoral researcher at the CNPRC and first author on the paper.
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Materials provided by University of California — Davis. Original written by Andy Fell. Note: Content may be edited for style and length.