Brain changes caused by Alzheimer’s different when disease inherited vs. developed sporadically

Over six million Americans suffer from Alzheimer’s disease, making it the most widespread form of dementia. The disease begins with mild memory loss and progresses to destroy the patients’ ability to execute the simplest tasks. Effective methods of treatment and prevention are desperately needed. Now, the findings of a study by researchers from the Indiana University School of Medicine and the MRC Laboratory of Molecular Biology in Cambridge, England could lead to new ways of fighting Alzheimer’s. 

Scientists say that the pathological changes caused by Alzheimer’s disease are different in people who have inherited the disease compared to people who have developed it sporadically.

Senile plaques are a key symptom of Alzheimer’s disease. They consist of a peptide called Amyloid-β 42 (Aβ 42). During their study, the researchers found that the type of Aβ 42 components — filaments — depends on how patients developed the disease.

“Type I filaments were found mostly in the brains of individuals with sporadic Alzheimer’s disease, and type II filaments were found in individuals with familial Alzheimer’s disease and other conditions,” the researchers write. 

“Although senile plaques have been known to be one of the main pathological changes in Alzheimer’s disease for over a century, their nature and composition has been gradually unraveled during the past four decades,” says study corresponding author Dr. Bernardino Ghetti, MD, lead researcher at the Indiana Alzheimer’s Disease Research Center, in a statement.

The research team conducted the study with ten participants, five with Alzheimer’s disease and five with different neurodegenerative conditions, using maps and 3D structures of the patients’ Aβ 42 to examine the filament structures. The researchers hope that by gaining knowledge about the structures, they can develop methods preventing their assembly, as well as better imaging. 

“This new knowledge of the filament structures provides deeper insights into the disease process in Alzheimer’s and may lead to the development of compounds that can prevent the disease by inhibiting filament formation as well as new methods for brain imaging,” Ghetti said. “This paper opens a new chapter for imaging and therapeutics.”

The study is published in Science.

Article written by Clio Rourke

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