Evidence map›Paper›PMID 41365832›Full record

ArticleMovement disorders : official journal of the Movement Disorder Society2026

Longitudinal Dynamics of Plasma Neurofilament Light Chain in Hereditary Spastic Paraplegia Type 11 (HSP-SPG11) and Type 15 (HSP-ZFYVE26).

Habibah A P Agianda, Julian E Alecu, Amy Tam, Hyo-Min Kim, Joshua Rong, Nicole Battaglia, Kaitlyn Warren, Rebekah Mannix, Nunzio Setola, Melissa Barghigiani and 8 more

Abstract read
In one paragraph

Article in Movement disorders : official journal of the Movement Disorder Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors.

Habibah A P AgiandaMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID https://orcid.org/0000-0002-5346-5026
Julian E AlecuMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Amy TamMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Hyo-Min KimMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Joshua RongMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID https://orcid.org/0009-0001-5277-5794
Nicole BattagliaMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Kaitlyn WarrenDivision of Emergency Medicine, Department of Pediatrics, Boston Children's Hospital, Boston, Massachusetts, USA.
Rebekah MannixDivision of Emergency Medicine, Department of Pediatrics, Boston Children's Hospital, Boston, Massachusetts, USA.
Nunzio SetolaMolecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy.
Melissa BarghigianiMolecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy.
Grace YoonDivision of Clinical and Metabolic Genetics, Department of Paediatrics, The Hospital for Sick Children, Toronto, Ontario, Canada.
Yoshihisa TakiyamaDepartment of Neurology, Fuefuki Central Hospital, Yamanashi, Japan.
Jangsup MoonDepartment of Genomic Medicine, Department of Neurology, Seoul National University Hospital, Seoul, South Korea.ORCID https://orcid.org/0000-0003-1282-4528
Katerina BernardiMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Kathryn YangMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID https://orcid.org/0009-0004-6892-5189
Luca SchierbaumMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Filippo Maria SantorelliMolecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy.ORCID https://orcid.org/0000-0002-1359-9062
Darius Ebrahimi-FakhariMovement Disorders Program, Department of Neurology, Boston Children's Hospital, Harvard Medical School, Boston, Massachusetts, USA.ORCID https://orcid.org/0000-0002-0026-4714

Funding

Spastic Paraplegia Centers of Excellence Research Network (SP-CERN) - RDCRCU54NS148312 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI Darius Ebrahimi-Fakhari · 2025 to 2026
$5.0M
Development of a Translational Research Platform to Understand and treat Defective Protein Trafficking in Childhood-Onset Hereditary Spastic ParaplegiaK08NS123552 · NINDS · BOSTON CHILDREN'S HOSPITAL · PI EBRAHIMI-FAKHARI, DARIUS · 2021 to 2025
$1.1M
EURO-HSPNINDS NIH HHS 1U54NS148312NINDS NIH HHS K08 NS123552NINDS NIH HHS K08NS123552NINDS NIH HHS U54 NS148312Spastic Paraplegia Foundation
6 · The paper itself

Abstract

backgroundHSP-SPG11 and HSP-ZFYVE26 are autosomal-recessive forms of hereditary spastic paraplegias (HSPs). As therapeutic trials emerge, validated biomarkers are critically needed.

objectivesTo evaluate plasma neurofilament light chain (pNfL) as a biomarker for neurodegeneration and disease progression.

methodsWe analyzed pNfL levels in 57 patients (36 HSP-SPG11, 21 HSP-ZFYVE26) and matched controls using single-molecule array technology. Longitudinal clinical and biomarker data were collected over 5 years.

resultsBaseline pNfL levels were significantly elevated in patients: 33.85 pg/mL (IQR 25.15-47.38) in HSP-SPG11, 46.70 pg/mL (IQR 29.95-54.84) in HSP-ZFYVE26, and 4.90 pg/mL (IQR 3.48-6.90) in controls (P < 0.001). No significant difference was observed between HSP-SPG11 and HSP-ZFYVE26. In matched pair analysis, pNfL showed inverse correlation with age (ρ = -0.463, P < 0.001). Baseline pNfL did not predict future clinical progression.

conclusionsElevated pNfL reflects early neuroaxonal injury in HSP-SPG11 and HSP-ZFYVE26; however, it could not be used as a surrogate for disease progression. © 2025 International Parkinson and Movement Disorder Society.

Indexed as

Neurofilament ProteinsSpastic Paraplegia, HereditaryAdolescentAdultBiomarkersDisease ProgressionFemaleHumansLongitudinal StudiesMaleMiddle AgedProteinsYoung AdultBiomarkersneurofilament protein LNeurofilament ProteinsProteinsSPG11 protein, humanaxonal degenerationbiomarkerhereditary spastic paralysisneurofilament light chainspasticity

Identifiers

PMID41365832
PMCPMC13502287

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.