A new study of an inherited form of Alzheimer’s disease shows that a protein called GFAP is a possible biomarker for very early stages of the disease. The study, conducted by researchers at Karolinska Institutet and published in the journal Brain, could one day lead to an early diagnosis. Alzheimer’s disease begins decades before any symptoms, such as memory loss, begin to show. As a result, early detection increases the chances of slowing the disease with medication.
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“Our results suggest that GFAP, a putative biomarker for activated immune cells in the brain, reflects changes in the brain due to Alzheimer’s that occur before tau protein accumulation and measurable neuronal damage,” says first author of the study. study Charlotte Johansson, PhD candidate in the Department of Neurobiology, Care Sciences and Society, Karolinska Institutet, Sweden. “In the future, it could be used as a non-invasive biomarker for the early activation of immune cells such as astrocytes in the central nervous system, which may be valuable for the development of new drugs and for diagnosing cognitive diseases.”
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In Alzheimer’s disease — which causes 60 to 70 percent of all cases of dementia, according to the Swedish Brain Foundation — nerve cells in the brain degenerate due to the abnormal buildup of amyloid-beta and tau proteins. As more brain neurons are damaged, this manifests itself in the dysfunction of cognitive functions such as memory and speech. The disease progresses insidiously and biological changes in the brain begin as early as 20 to 25 years before memory loss and other cognitive symptoms become apparent. The sooner a patient is diagnosed correctly, the sooner they will be offered the right treatment. Researchers at Karolinska Institutet and their colleagues at Landspitali University Hospital in Iceland, the University of Gothenburg and University College London in the UK studied biomarkers in blood for very early pathological changes in a rare, inherited form of the disease Alzheimer’s disease which accounts for less than 1% of all cases. Individuals with a parent with Alzheimer’s disease caused by a mutation have a 50% risk of developing the disease themselves.
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For their study, the researchers analyzed 164 blood plasma samples from 33 mutation carriers and 42 relatives without the hereditary predisposition. The data was collected between 1994 and 2018. Their results reveal clear changes of different blood protein concentrations in mutation carriers. “The first change we observed was an increase in GFAP (glial fibrillary acid protein) about ten years before the first symptoms of the disease,” says the study’s last author. Caroline Graff, professor in the Department of Neurobiology, Nursing Sciences and Society, Karolinska Institutet. “This was followed by increased concentrations of P-tau181 and, subsequently, NfL (neurofilament light protein), which we already know to be
directly associated with the extent of neuronal damage in the brain of Alzheimer’s sufferers. This discovery about GFAP improves the chances of an early diagnosis.”
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