![Synergistic effect between [18F]florbetapir SUVR and CSF p-tau drives [18F]FDG uptake decline in limbic regions. Statistical parametric maps, after correcting for multiple comparisons (false discovery rate corrected at P<0.001), overlaid in a structural MRI scan, reveal areas in which 24-month [18F]FDG uptake decline occurs as a function of the synergistic interaction between baseline [18F]florbetapir SUVR and CSF p-tau measurements. Significant interactive effects were observed in the basal and mesial temporal, orbitofrontal, and anterior and posterior cingulate cortices. The analysis was corrected for age, gender and APOE ε4 status. CSF, cerebrospinal fluid; [18F]FDG, [18F]fluorodeoxyglucose; MRI, magnetic resonance imaging; p-tau, phosphorylated tau; SUVR, standardized uptake value ratio.](https://www.nature.com/mp/journal/vaop/ncurrent/images/mp201637f2.jpg)
Synergistic effect between [18F]florbetapir SUVR and CSF p-tau drives [18F]FDG uptake decline in limbic regions. Statistical parametric maps, after correcting for multiple comparisons (false discovery rate corrected at P<0.001), overlaid in a structural MRI scan, reveal areas in which 24-month [18F]FDG uptake decline occurs as a function of the synergistic interaction between baseline [18F]florbetapir SUVR and CSF p-tau measurements. Significant interactive effects were observed in the basal and mesial temporal, orbitofrontal, and anterior and posterior cingulate cortices. The analysis was corrected for age, gender and APOE ε4 status. CSF, cerebrospinal fluid; [18F]FDG, [18F]fluorodeoxyglucose; MRI, magnetic resonance imaging; p-tau, phosphorylated tau; SUVR, standardized uptake value ratio.
Dr. Pedro Rosa-Neto, a clinician scientist at the Douglas and assistant professor of Neurology, Neurosurgery and Psychiatry at McGill University, reports for the first time evidence that the interaction between amyloid and tau proteins drives brain damage in cognitively intact individuals.
“We specifically found that both proteins mutually enhance their individual toxic effects and cause a brain dysfunction considered to be a signature of AD. This finding challenges previous polarized theories that a single protein abnormality was the major driving force of disease progression,” explains Dr. Rosa-Neto.
Summary of image analysis methods.
This research also points toward new therapeutic strategies to mitigate the progression of AD. “Until now, therapeutic clinical trials have targeted a single pathological process. Our result paves the way for new therapeutic strategies for prevention or stabilization of AD. For example, combination therapies should be used simultaneously against both amyloid and tau protein accumulation,” says Dr. Tharick A. Pascoal.
Rosa-Neto’s team analyzed the performances of 120 cognitively intact individuals over 2 years (equal gender distribution; average age 75). By measuring amyloid levels using PET scans and tau proteins through cerebrospinal fluid analysis, the researchers were able to identify the patients at risk of brain damage associated with AD.
According to the World Health Organization, Alzheimer’s disease is the most common cause of dementia, affecting more than 30 million people worldwide in 2015. In 2011, 747,000 Canadians were living with Alzheimer’s disease and other forms of dementia, and the combined direct (medical) and indirect (lost earnings) costs of dementia amounted to $33 billion (Alzheimer Society of Canada). http://www.mcgill.ca/newsroom/channels/news/alzheimers-disease-it-takes-two-proteins-tango-260514
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