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Henrik Zetterberg. Alzheimer’s disease Kaj Blennow, Mony J de Leon, Henrik Zetterberg Alzheimer’s disease is the most common cause of dementia.
Amyloid beta (Aβ), the key component of extracellular senile plaques in Alzheimer’s disease (AD) brains, is produced from amyloid precursor protein (APP) by proteolytic processing via the β-site APP-cleaving enzyme 1 (BACE1) and the γ-secretase complex. Henrik Zetterberg. Alzheimer’s disease (AD) is a clinically and pathophysiologically heterogeneous complex neurodegenerative disease (ND). He has published more than 1100 scientific articles and has received numerous awards. Isolating toxic and non-toxic Aβ plaques regions and looking for differences in their Aβ composition.Prof Henrik Zetterberg’s team is working to address these issues by developing ultrasensitive new tests to help measure molecular changes in body fluids of people with Alzheimer's disease and other neurodegenerative conditions.

Explore whether amyloid build-up in AD is caused by an imbalance in the production and clearance of specific Aβ isoforms.

UK Dementia Research Institute at UCL, London, UK.

However, the hypothesis has been challenged by negative results in several phase III clinical trials aimed at inhibiting Aβ production (secretase inhibitors) or increasing its clearance from the brain (anti-Aβ immunotherapy).

Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, London, UK. The specific aims are to:The recent negative trial outcomes have also highlighted the need for more translational research on disease models to study AD pathogenesis, screen for and evaluate new drug candidates and establish pharmacodynamic biomarkers to verify target engagement and translate model findings to valid readouts in clinical trials. Along similar lines, we need new biomarker tools to study the pathophysiological relevance of and cellular responses to non-Aβ pathologies that are common in AD and highly relevant to several other neurodegenerative diseases, namely tau, α-synuclein and TDP-43.3. But these may simply reflect the currently inadequate tests of the Aβ cascade hypothesis in terms of molecular and clinical end-points. He has developed new diagnostic tests for Alzheimer’s disease, as well as new preclinical models, and has shown that (i) amyloid pathology precedes tau pathology by around five years during the Alzheimer’s disease process in humans, (ii) altered amyloid homeostasis in the brain is evident already in pre-symptomatic stages of the disease, and (iii) the diagnostic usefulness of Alzheimer’s biomarkers decreases with age due to increased prevalence of preclinical Alzheimer neuropathology.


Lancet Neurology, Journal article 2020 Journal article Ultrasensitive assays for pathology-specific forms of TDP-43, α-synuclein and tau proteins.2. Get the latest news and updates from the Foundation directly to your inbox.With a background in molecular biology and clinical chemistry, Henrik Zetterberg, MD, PhD, has spent the last 10 years focusing on the development of biomarkers for Alzheimer’s disease, Parkinson’s disease and other brain disorders. The team also hope to uncover previously unknown biological changes in body fluids, which may give an indication of harmful processes taking place in the brain much earlier in the disease timecourse.1. Furthermore, trials in pre-clinical disease stages will at least be needed to address the Aβ cascade hypothesis – these trials bring greater importance to biomarkers since, by definition, the clinical effects are difficult or slow to discern in a population that is not clinically affected.Diagnostic and prognostic biomarkers, Alzheimer’s disease, clinical trials, amyloid beta© 2020 UK Dementia Research Institute4. Alzheimer’s disease. With a background in molecular biology and clinical chemistry, Henrik Zetterberg, MD, PhD, has spent the last 10 years focusing on the development of biomarkers for Alzheimer’s disease, Parkinson’s disease and other brain disorders.