BU99008 traces reactive astrogliosis, a marker that provides early, rapid Alzheimer’s detection.
A new PET tracer – BU99008 – could play a key role in detecting the early stages of Alzheimer’s disease, according to newly published research.
Changes to brain function caused by Alzheimer’s can begin as early as 10-to-20 years before the cognitive decline is noticed clinically. Such early neurological alterations make the identification of early disease markers that much more critical.
In a new study published April 22 in Molecular Psychiatry, a multi-institutional team of investigators from Karolinska Institutet, Uppsala University, and Indiana University School of Medicine discussed how BU99008 can be used to trace reactive astrogliosis, a marker that can provide an early, rapid response to the progression of the disease.
Astrocytes, the team said, are the most important homeostatic cells present in the central nervous system, and they perform a myriad of functions to maximize cerebral function and cellular energy supply.
“Our study shows that BU99008 can detect important reactive astrocytes with good selectivity and specificity, making it a potentially important clinical astrocytic PET tracer,’” said first author Amit Kumar, Ph.D., a researcher in the neurobiology, care sciences, and society department at Karolinska Institutet. “The results can improve our knowledge of the role played by reactive astrogliosis in Alzheimer’s disease.”
For their study, the team examined brain tissue from six patients who died from Alzheimer’s, as well as seven other healthy individuals who died from other causes. Their results shed light on how the binding properties of BU99008 compare with other existing astrocytic Alzheimer’s disease brain biomarkers.
“As far as we can judge, this is the first time that BU99008 could visualize reactive astrogliosis in Alzheimer’s disease brain,” said principal investigator Agneta Nordberg, M.D., Ph.D., professor of clinical neuroscience at Karolinska Institutet. “The results can have broad clinical implications that cover other disorders of reactive astroglial dysfunction.”
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