CEEPC/IPM/CMSC - Abstrakt prezentace

(CEEPC/IPM/CMSC 2022 - ThS-06)
Comprehensive metabolomic and lipidomic study of tauopathy and Alzheimer's disease patients

Dana Dobešová 1 *, Aleš Kvasnička 1, Eliška Ivanovová 1, Barbora Piskláková 1, Dominika Olešová 2, Petra Majerová 2, Andrej Kováč 2, David Friedecký 1

  1. Laboratory for Inherited Metabolic Disorders, Department of Clinical Biochemistry, University Hospital Olomouc
  2. Institute of Neuroimmunology, Slovak Academy of Sciences, Dubravska cesta 9, 84510, Bratislava, Slovakia


Alzheimer's disease (AD) belongs to the group of tauopathies, which are classified as neurodegenerative disorders. AD is manifested by dementia, cognitive loss, and other neurological impairments. Currently, more than 55 million people worldwide have dementia and 60-70% of them have been diagnosed with AD. One of the causes of AD development is the accumulation of structurally disrupted tau protein, which aggregates into insoluble neurofibrillary tangles that disrupt neurons.
The aim of this study was to describe the pathological processes in AD patients and five cohorts of tauopathy and to compare them with the profile of healthy subjects. The tauopathy cohorts were as follows: Progressive supranuclear palsy (PSP), Corticobasal degeneration (CBD), Behavioral variant of frontotemporal dementia (bvFTD) and Semantic variant/ Non-fluent agrammatic variant of primary progressive aphasia (svPPA/ nfaPPA). Cerebrospinal fluid samples were obtained from patients and controls. A combination of targeted metabolomic and lipidomic approach was chosen for an objective assessment of the study.
The metabolic and lipid profile revealed differences predominantly in tauopathies compared to controls. Elevated levels dominated in several amino acids, acylcarnitines, lysophosphatidylcholines, ceramides and sphingomyelins. These observations are probably related to the anti-inflammatory processes [1] or the loosening of phospholipid membranes due to neurodegeneration [2]. Subsequently, this may have resulted from impaired mitochondrial function and the breakdown of other cellular components [3]. The findings significantly contribute to the understanding of the pathobiochemistry of AD and tauopathies and also affect the frontiers of diagnosis and treatment.

* Korespondující autor: dobesova.dana147@gmail.com


  1. Yan X. et al.: Front. Neurosci. 14, (2020).
  2. Wang S. et al.: Molecular Neurodeg. 16(26), (2021).
  3. Gonzalez-Covarrubias V. et al.: Metabolites 12(2), (2022).


This project was supported by the Doctoral Study Grant (DSGC-2021-0098) of Palacký University in Olomouc and Agency for Medical Research of the Czech Republic (NU20-08-00367).

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