Signs have been discovered in the brain of the early stages of Alzheimer’s disease, with the potential to allow earlier detection of the disease, Swedish researchers have reported.
Novel forms of abnormal tau protein were identified by a team at the University of Gothenburg, Sweden. These become abnormal before cognitive problems are apparent, they report.
The researchers found specific forms of phosphorylated tau (p-tau) that show minute increases in cerebrospinal fluid and blood, that were linked to the individual later developing Alzheimer’s.
They then created techniques to measure these biological markers and confirmed their effectiveness in human studies. In one study of 381 people, a third had abnormal p-tau without any measurable cognitive problems.
The p-tau markers correlated well with abnormalities in cerebrospinal fluid and blood samples, and further studies showed that these p-tau markers continue to grow all the way to the late stages of dementia.
Dr Kaj Blennow said: “A possible way to improve the chances of future therapies is to test them on people in the very early stages of the disease with elusive biological changes but lacking clinical symptoms including memory failings. Candidate drug trials have not been too successful.
“The practical challenge, however, is that these very tiny initial changes are incredibly difficult to measure reliably. This compromises our chances to identify and recruit preclinical Alzheimer’s disease patients for clinical trials.”
Details were published in Alzheimer’s & Dementia on Monday (30 November).
Co-author Dr Thomas Karikari added: “The remarkable findings show that the new highly sensitive tools capture the earliest Alzheimer disease changes in the brain in clinically normal people. These tools therefore have the potential to advance population screening and clinical trials.”
Karikari, T. K. et al. Head-to-head comparison of clinical performance of CSF phospho-tau T181 and T217 biomarkers for Alzheimer’s disease diagnosis. Alzheimer’s & Dementia 20 November 2020 doi: 10.1002/alz.12236
Leave a Reply