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000285033 037__ $$aDZNE-2026-00158
000285033 041__ $$aEnglish
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000285033 1001_ $$aKessler, Christoph$$b0
000285033 245__ $$aSerum NfL, but not GFAP, differentiates primary lateral sclerosis from adrenomyeloneuropathy and hereditary spastic paraplegia type 4.
000285033 260__ $$aAbingdon$$bTaylor Francis Group$$c2026
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000285033 520__ $$aNeurodegenerative upper motor neuron (UMN) syndromes ranging from primary lateral sclerosis (PLS) to pure and complicated types of hereditary spastic paraplegia (HSP) remain challenging to differentiate clinically, especially in the early stages of disease. As they share the hallmark of spastic paraparesis, easily accessible biomarkers are warranted to facilitate an early diagnosis.We examined serum neurofilament light chain (sNfL) and serum glial fibrillary acidic protein (sGFAP) as diagnostic biomarkers to differentiate PLS from HSP, represented by two paradigmatic subtypes: SPG4, the most common type of pure HSP, and adrenomyeloneuropathy (AMN), a common complicated form of HSP. In addition to sNfL and sGFAP raw levels, we used age-adjusted z-scores to account for age-related biomarker level increases.In our cohort of 18 PLS patients, 18 AMN patients, 25 SPG4 patients and 60 controls, sNfL z-scores were higher in PLS than in SPG4 (p < 0.001), AMN (p = 0.03), and controls (p < 0.001). Furthermore, sNfL z-scores allowed distinguishing PLS from SPG4 (AUC 0.82, 95% CI 0.67-0.98) and-slightly less accurate-from AMN (AUC 0.77, 95% CI 0.60-0.95). sGFAP z-scores did not differ significantly between groups.Our study suggests that serum NfL, but not GFAP, is a potential diagnostic biomarker in degenerative UMN diseases and may help to differentiate PLS from pure and complicated forms of HSP. Our results indicate that axonal degeneration-the source of NfL release-is predominant over astrocytic pathology-the source of GFAP release-in PLS, AMN, and SPG4.
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000285033 650_7 $$2Other$$aBiomarker
000285033 650_7 $$2Other$$aGFAP
000285033 650_7 $$2Other$$aHSP
000285033 650_7 $$2Other$$aNfL
000285033 650_7 $$2Other$$aPLS
000285033 650_7 $$2NLM Chemicals$$aNeurofilament Proteins
000285033 650_7 $$2NLM Chemicals$$aGlial Fibrillary Acidic Protein
000285033 650_7 $$2NLM Chemicals$$aneurofilament protein L
000285033 650_7 $$2NLM Chemicals$$aBiomarkers
000285033 650_7 $$2NLM Chemicals$$aGFAP protein, human
000285033 650_2 $$2MeSH$$aHumans
000285033 650_2 $$2MeSH$$aMale
000285033 650_2 $$2MeSH$$aFemale
000285033 650_2 $$2MeSH$$aMiddle Aged
000285033 650_2 $$2MeSH$$aSpastic Paraplegia, Hereditary: blood
000285033 650_2 $$2MeSH$$aSpastic Paraplegia, Hereditary: diagnosis
000285033 650_2 $$2MeSH$$aNeurofilament Proteins: blood
000285033 650_2 $$2MeSH$$aGlial Fibrillary Acidic Protein: blood
000285033 650_2 $$2MeSH$$aAdult
000285033 650_2 $$2MeSH$$aAdrenoleukodystrophy: blood
000285033 650_2 $$2MeSH$$aAdrenoleukodystrophy: diagnosis
000285033 650_2 $$2MeSH$$aBiomarkers: blood
000285033 650_2 $$2MeSH$$aDiagnosis, Differential
000285033 650_2 $$2MeSH$$aAged
000285033 650_2 $$2MeSH$$aYoung Adult
000285033 650_2 $$2MeSH$$aCohort Studies
000285033 7001_ $$0P:(DE-2719)2814101$$aWilke, Carlo$$b1$$udzne
000285033 7001_ $$0P:(DE-2719)2811940$$aHengel, Holger$$b2
000285033 7001_ $$0P:(DE-2719)2811827$$aRattay, Tim W$$b3$$udzne
000285033 7001_ $$aMaleska Maceski, Aleksandra$$b4
000285033 7001_ $$aKuhle, Jens$$b5
000285033 7001_ $$0P:(DE-2719)2810795$$aSchöls, Ludger$$b6$$udzne
000285033 7001_ $$0P:(DE-2719)2812018$$aSchüle, Rebecca$$b7$$eLast author$$udzne
000285033 773__ $$0PERI:(DE-600)2705061-0$$a10.1080/21678421.2025.2557936$$gVol. 27, no. 1-2, p. 110 - 117$$n1-2$$p110 - 117$$tAmyotrophic lateral sclerosis & frontotemporal degeneration$$v27$$x2167-8421$$y2026
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