Markus Otto

Prof. Dr. Markus Otto


Research Focus & Metrics

Academic Career Length

19Years (2008-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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31 August 2018 in Nature Reviews Neurology
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Journal Article
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MKMichael Khalil
Michael Khalil
CTCharlotte E. Teunissen
Charlotte E. Teunissen
MOMarkus Otto
Markus Otto
FPFredrik Piehl
Fredrik Piehl
MSMaria Pia Sormani
Maria Pia Sormani
JKJens Kuhle
Jens Kuhle

3 February 2022 in Nature Reviews Neurology
Verified
Journal Article
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AAAhmed Abdelhak
Ahmed Abdelhak
MFMatteo Foschi
Matteo Foschi
SASamir Abu-Rumeileh
Samir Abu-Rumeileh
JYJohn K. Yue
John K. Yue
LDLucio D’anna
Lucio D’anna
Hayrettin TumaniHayrettin Tumani
Hayrettin Tumani

22 April 2019 in Alzheimer's Research & Therapy
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Journal Article
Open access
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OHOskar Hansson
Oskar Hansson
SLSylvain Lehmann
Sylvain Lehmann
MOMarkus Otto
Markus Otto
HZHenrik Zetterberg
Henrik Zetterberg
PLPiotr Lewczuk
Piotr Lewczuk
The cerebrospinal fluid (CSF) biochemical markers (biomarkers) Amyloidβ 42 (Aβ42), total Tau (T-tau) and Tau phosphorylated at threonine 181 (P-tau181) have proven diagnostic accuracy for mild cognitive impairment and dementia due to Alzheimer’s Disease (AD). In an effort to improve the accuracy of an AD diagnosis, it is important to be able to distinguish between AD and other types of dementia (non-AD). The concentration ratio of Aβ42 to Aβ40 (Aβ42/40 Ratio) has been suggested to be superior to the concentration of Aβ42 alone when identifying patients with AD. This article reviews the available evidence on the use of the CSF Aβ42/40 ratio in the diagnosis of AD. Based on the body of evidence presented herein, it is the conclusion of the current working group that the CSF Aβ42/40 ratio, rather than the absolute value of CSF Aβ42, should be used when analysing CSF AD biomarkers to improve the percentage of appropriately diagnosed patients.

12 April 2024 in Nature Reviews Neurology
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Journal Article
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MKMichael Khalil
Michael Khalil
CTCharlotte E. Teunissen
Charlotte E. Teunissen
SLSylvain Lehmann
Sylvain Lehmann
MOMarkus Otto
Markus Otto
FPFredrik Piehl
Fredrik Piehl
JKJens Kuhle
Jens Kuhle

25 August 2020 in Journal of Neurology
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Journal Article
Open access
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SASamir Abu-Rumeileh
Samir Abu-Rumeileh
AAAhmed Abdelhak
Ahmed Abdelhak
MFMatteo Foschi
Matteo Foschi
HTHayrettin Tumani
Hayrettin Tumani
MOMarkus Otto
Markus Otto
Since coronavirus disease-2019 (COVID-19) outbreak in January 2020, several pieces of evidence suggested an association between the spectrum of Guillain–Barré syndrome (GBS) and severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Most findings were reported in the form of case reports or case series, whereas a comprehensive overview is still lacking. We conducted a systematic review and searched for all published cases until July 20th 2020. We included 73 patients reported in 52 publications. A broad age range was affected (mean 55, min 11–max 94 years) with male predominance (68.5%). Most patients showed respiratory and/or systemic symptoms, and developed GBS manifestations after COVID-19. However, asymptomatic cases for COVID-19 were also described. The distributions of clinical variants and electrophysiological subtypes resemble those of classic GBS, with a higher prevalence of the classic sensorimotor form and the acute inflammatory demyelinating polyneuropathy, although rare variants like Miller Fisher syndrome were also reported. Cerebrospinal fluid (CSF) albuminocytological dissociation was present in around 71% cases, and CSF SARS-CoV-2 RNA was absent in all tested cases. More than 70% of patients showed a good prognosis, mostly after treatment with intravenous immunoglobulin. Patients with less favorable outcome were associated with a significantly older age in accordance with previous findings regarding both classic GBS and COVID-19. COVID-19-associated GBS seems to share most features of classic post-infectious GBS and possibly the same immune-mediated pathogenetic mechanisms. Nevertheless, more extensive epidemiological studies are needed to clarify these issues.

24 December 2018 in Journal of Alzheimer’s Disease
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Journal Article
Closed access
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POPatrick Oeckl
Patrick Oeckl
SHSteffen Halbgebauer
Steffen Halbgebauer
SASarah Anderl-Straub
Sarah Anderl-Straub
PSPetra Steinacker
Petra Steinacker
AHAndré M. Huss
André M. Huss
MOMarkus Otto
Markus Otto
Reliable blood biomarkers for Alzheimer’s disease (AD) are missing. We measured astroglial GFAP in patients with AD ( n = 28), frontotemporal dementia (bvFTD, n = 35), Parkinson’s disease ( n = 11), Lewy body dementias ( n = 19), and controls ( n = 34). Serum GFAP was increased in AD ( p < 0.001) and DLB/PDD ( p < 0.01), and cerebrospinal fluid GFAP was increased in all neurodegenerative diseases ( p < 0.001). Serum GFAP correlated with the Mini-Mental State Examination score ( r= –0.42, p < 0.001) and might be a follow-up marker in clinical trials. Sensitivity and specificity of serum GFAP for AD versus bvFTD was 89% and 79% and might be the first blood biomarker in the differential diagnosis of AD and bvFTD.