This new finding could lead to the development of novel therapies to prevent the eventual onset of Alzheimer's.
Using mice modified to develop Alzheimer's disease, the research team at Mount Sinai School of Medicine found that when β-amyloid, an abnormal protein linked to Alzheimer's disease, starts to become detectable in the brain in its soluble toxic form, the mitochondria, or "power plants" of the cell where glucose is converted into energy, became impaired.
Within the equivalent of about 20 human years, mice with decreased energy metabolism developed signs of Alzheimer's disease such as cognitive defects and impairment of the synaptic terminal, the area of brain cells important in memory formation.
"This evidence in mice validates that the diagnosis of probable Alzheimer's disease may be the end result of impairment in brain cell energy production," said Giulio M. Pasinetti, The Saunder Family Professor in Neurology, and Professor of Psychiatry, Geriatrics, and Adult Development at Mount Sinai School of Medicine. "Identifying that mitochondrial impairment is evident years earlier than cognitive defects is a major breakthrough."
"This new evidence could revolutionize the way we design interventions," said Doctor Merina T. Varghese, co-author of the study. "This study sets the stage for the development of potential novel preventions or therapies to apply in humans, even when they have normal cognitive function, to prevent the eventual onset of Alzheimer's disease."
MEDICA.de; Source: The Mount Sinai Hospital / Mount Sinai School of Medicine