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The Sahlgrenska Academy is the faculty of health sciences at the University of Gothenburg. Education and research are conducted within the fields of pharmacy, medicine, odontology and health care sciences. About 4000 undergraduate students and 1000 postgr
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Scientific Advisory Board | Alzheon
Kaj Blennow, MD, PhD
Professor of Clinical Neurochemistry, University of Gothenburg, Sweden
Head of Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Gothenburg, Sweden
Alzheimer's Association Partnerships | Biomarker Projects
To address these issues, Kaj Blennow, M.D., Professor of Clinical Neurochemistry at the University of Gothenburg (Sweden), drafted a survey to be completed by European AD investigators engaged in CSF assays for AD research or practice.
Dr. Blennow invited representatives from Washington University, St Louis, to develop the survey further and introduce it to the Alzheimer's Disease Centers (ADCs).
Kaj Blennow, MD, PhD
Kaj Blennow, MD, PhD is a professor at Sahlgrenska University Hospital in Goteborg, Sweden.
conducts research on the mechanisms behind neurological disorders and over the past twenty (20) years, he
has developed biochemical tests for Alzheimer's disease.
He is a world-renowned researcher and clinician in both concussion and Alzheimer's disease.
Kaj Blennow, University ...
Kaj Blennow, University of Gothenburg, Sweden
A recent review article in Alzheimer's ...
A recent review article in Alzheimer's and Dementia discusses the current state of cerebrospinal fluid-borne markers for Alzheimer disease.2 Tests that identify proteins in the CSF could be very specific to Alzheimer disease because the fluid directly interacts with brain tissue.3 According to first author, Kaj Blennow, MD, PhD, Professor of Clinical Neurochemistry at the Sahlgrenska University Hospital in Mölndal, Sweden, CSF is potentially better than blood since "a brain protein will be diluted in the larger blood volume, metabolized and degraded.
explains "They have been evaluated in hundreds of papers and very consistently show that more than 85%-90% of AD (and prodromal AD) cases have low Abeta42 and high total-tau and phospho-tau."
Levels of CSF amyloid-beta seem to decrease as post-mortem or biopsied brain levels increase, so it seems that the protein may deposit itself in the brain and while it correspondingly decreases in the fluid.
CSF phosphorylated tau levels also correspond with the amount of neurofibrillary tangles found in a later autopsy.
In addition, high levels of total tau in the CSF seem to indicate that mild cognitive impairment will quickly progress to full Alzheimer dementia.
Unfortunately, the markers seem to be only good in the early stages of the disease.
explains: "it seems that the AD biomarkers reach a plateau very early in disease progression, and thus do not change with progression."
Researchers may have another problem with developing a clinical test: the methods being used are not the same in every lab.
The development of consistent assays is a high current priority in this field.
According to Dr Blennow
"what is needed is more work on standardization, both the analytical part and assay production, so that we can get uniform values between labs.