Journal Article

DZNE-2026-00901

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png Impact of Plasma p-tau181 on Cognition, Motor Phenotypes, and Disease Course in ALS.

Kasper, E. (First author)DZNE* ; Lehto, A.DZNE* ; Nordmann, N. ; Peters, O.DZNE* ; Hellmann-Regen, J. D. N.DZNE* ; Priller, J.DZNE* ; Spruth, E. J.DZNE* ; Petzold, G. C.DZNE* ; Vogt, I.DZNE* ; Weydt, P.DZNE* ; Bernsen, S.DZNE* ; Dinter, E.DZNE* ; Falkenburger, B.DZNE* ; Günther, R.DZNE* ; Düzel, E.DZNE* ; Glanz, W.DZNE* ; Synofzik, M.DZNE* ; Beichert, L.DZNE* ; Spottke, A.DZNE* ; Wagner, M.DZNE* ; Brosseron, F.DZNE* ; Schmid, M. C.DZNE* ; Schneider, A.DZNE* ; Teipel, S.DZNE* ; Prudlo, J.DZNE* ; Hermann, A. (Last author)DZNE*

2026
Wiley Chichester [u.a.]

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Please use a persistent id in citations: doi:10.1002/acn3.70423

Abstract: Phosphorylated tau181 (p-tau181), an Alzheimer's disease biomarker, was recently evaluated in amyotrophic lateral sclerosis (ALS). We investigated plasma p-tau181 in 202 ALS/ALS-FTD patients and 94 healthy controls, assessing cognitive performance, motor function, and longitudinal dynamics. Plasma p-tau181 and NfL were significantly elevated in ALS, with p-tau181 increasing over 1 year while NfL remained stable. Neither marker correlated with cognitive performance, and only NfL was associated with disease severity and progression. Plasma p-tau181 was higher in patients with predominant lower motor neuron involvement. The results indicate that p-tau181 reflects peripheral processes in ALS, providing a complementary, mechanistically distinct biomarker from NfL.

Keyword(s): Humans (MeSH) ; Amyotrophic Lateral Sclerosis: blood (MeSH) ; Amyotrophic Lateral Sclerosis: physiopathology (MeSH) ; Amyotrophic Lateral Sclerosis: complications (MeSH) ; tau Proteins: blood (MeSH) ; Female (MeSH) ; Disease Progression (MeSH) ; Male (MeSH) ; Aged (MeSH) ; Middle Aged (MeSH) ; Biomarkers: blood (MeSH) ; Phosphorylation (MeSH) ; Frontotemporal Dementia: blood (MeSH) ; Frontotemporal Dementia: physiopathology (MeSH) ; Frontotemporal Dementia: complications (MeSH) ; Neurofilament Proteins: blood (MeSH) ; Longitudinal Studies (MeSH) ; Cognitive Dysfunction: etiology (MeSH) ; Cognitive Dysfunction: blood (MeSH) ; Cognitive Dysfunction: physiopathology (MeSH) ; Alzheimer disease ; amyotrophic lateral sclerosis ; plasma p‐tau181 ; tau Proteins ; Biomarkers ; MAPT protein, human ; Neurofilament Proteins

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Contributing Institute(s):

1. Translational Neurodegeneration (AG Hermann)
2. Clinical Dementia Research (Rostock /Greifswald) (AG Teipel)
3. Biomarker-Assisted Early Detection of Dementias (AG Peters)
4. Interdisciplinary Dementia Research (AG Endres)
5. Translational Neuropsychiatry (AG Priller)
6. Vascular Neurology (AG Petzold)
7. Clinical Research Platform (CRP) (AG Spottke)
8. Clinical Research Coordination (Clinical Research (Bonn))
9. Clinical Neuroimaging (AG Radbruch)
10. Translational Parkinson Research (AG Falkenburger)
11. Clinical Neurophysiology and Memory (AG Düzel)
12. Parkinson Genetics (AG Gasser)
13. Clinical Research Platform (CRP) (Clinical Research Platform (CRP))
14. Neuropsychology (AG Wagner)
15. Neuroinflammation, Biomarker (AG Heneka)
16. Mathematics, statistics and informatics methods for support of population studies and clinical research (AG Schmid Bonn)
17. Translational Dementia Research (Bonn) (AG Schneider)

Research Program(s):

1. 353 - Clinical and Health Care Research (POF4-353) (POF4-353)

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Database coverage:
; ; Article Processing Charges ; Clarivate Analytics Master Journal List ; DEAL Wiley ; DOAJ Seal ; Ebsco Academic Search ; Essential Science Indicators ; Fees ; IF >= 5 ; JCR ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection

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