Evidence map›Paper›PMID 33522967›Full record

ArticleActa neuropathologica communications2021

Neuroligin-1 in brain and CSF of neurodegenerative disorders: investigation for synaptic biomarkers.

Elena Camporesi, Tammaryn Lashley, Johan Gobom, Juan Lantero-Rodriguez, Oskar Hansson, Henrik Zetterberg, Kaj Blennow, Bruno Becker

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
6.5field-weighted citation impact, top 2% of its field
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

31 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
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  5. Differences in blood levels of neuroligin-derived peptides in a cohort for early detection of Alzheimer's disease.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026
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  7. Frontiers in pharmacology · 2026
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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

8 authors at 3 institutions in 2 countries.

Elena CamporesiDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy At University of Gothenburg, Mölndal, Sweden. elena.camporesi@gu.se.ORCID 0000-0003-1044-0192
Tammaryn LashleyThe Queen Square Brain Bank for Neurological Disorders, Department of Clinical and Movement Neurosciences, UCL Institute of Neurology, London, UK.
Johan GobomDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy At University of Gothenburg, Mölndal, Sweden.
Juan Lantero-RodriguezDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy At University of Gothenburg, Mölndal, Sweden.
Oskar HanssonClinical Memory Research Unit, Department of Clinical Sciences, Lund University, Lund, Sweden.
Henrik ZetterbergDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy At University of Gothenburg, Mölndal, Sweden.
Kaj BlennowDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy At University of Gothenburg, Mölndal, Sweden.
Bruno BeckerDepartment of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy At University of Gothenburg, Mölndal, Sweden.
Sahlgrenska University Hospital · SELund University · SENational Hospital for Neurology and Neurosurgery · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synaptic pathology is a central event in Alzheimer's disease (AD) and other neurodegenerative conditions, and investigation of synaptic proteins can provide valuable tools to follow synaptic dysfunction and loss in these diseases. Neuroligin-1 (Nlgn1) is a postsynaptic cell adhesion protein, important for synapse stabilization and formation. Nlgn1 has been connected to cognitive disorders, and specifically to AD, as target of the synaptotoxic effect of amyloid-β (Aβ) oligomers and Aβ fibrils. To address changes in Nlgn1 expression in human brain, brain regions in different neurological disorders were examined by Western blot and mass spectrometry. Brain specimens from AD (n = 23), progressive supranuclear palsy (PSP, n = 11), corticobasal degeneration (CBD, n = 10), and Pick's disease (PiD, n = 9) were included. Additionally, cerebrospinal fluid (CSF) samples of AD patients (n = 43) and non-demented controls (n = 42) were analysed. We found decreased levels of Nlgn1 in temporal and parietal cortex (~ 50-60% reductions) in AD brains compared with controls. In frontal grey matter the reduction was not seen for AD patients; however, in the same region, marked reduction was found for PiD (~ 77%), CBD (~ 66%) and to a lesser extent for PSP (~ 43%), which could clearly separate these tauopathies from controls. The Nlgn1 level was reduced in CSF from AD patients compared to controls, but with considerable overlap. The dramatic reduction of Nlgn1 seen in the brain extracts of tauopathies warrants further investigation regarding the potential use of Nlgn1 as a biomarker for these neurodegenerative diseases.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBrainCase-Control StudiesCell Adhesion Molecules, NeuronalFemaleFrontal LobeGray MatterHumansMaleMiddle AgedParietal LobePick Disease of the BrainSupranuclear Palsy, ProgressiveTauopathiesCell Adhesion Molecules, Neuronalneuroligin 1Alzheimer’s diseaseNeuroligin-1Synapse lossTauopathies

Identifiers

PMID33522967
PMCPMC7852195
OpenAlexW3128734252

What OpenQuestion holds

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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 OpenQuestion graph.