Evidence map›Paper›PMID 35063468›Full record

ReviewBrain research2022

Neuroinflammation in Gaucher disease, neuronal ceroid lipofuscinosis, and commonalities with Parkinson's disease.

Laetitia Francelle, Joseph R Mazzulli

Open access · greenAbstract readReview
In one paragraph

Review in Brain research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Characterizing circulating biomarkers for childhood dementia disorders: A scoping review of clinical trials.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  5. Article
  6. Deciphering metabolic shifts in Gaucher disease type 1: a multi-omics study.Journal of molecular medicine (Berlin, Germany) · 2025
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. 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

2 authors at 1 institution in 1 country.

Laetitia FrancelleThe Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA.
Joseph R MazzulliThe Ken and Ruth Davee Department of Neurology, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. Electronic address: jmazzulli@northwestern.edu.
Northwestern University · US

Funding

Examining the role of glycosphingolipids in the progression and heterogeneity of synucleinopathiesRF1NS109157 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI MAZZULLI, JOSEPH R · 2019 to 2019
$1.9M
NINDS NIH HHS RF1 NS109157
6 · The paper itself

Abstract

Lysosomal storage diseases (LSDs) are rare genetic disorders caused by a disruption in cellular clearance, resulting in pathological storage of undegraded lysosomal substrates. Recent clinical and genetic studies have uncovered links between multiple LSDs and common neurodegenerative diseases such as Parkinson's disease (PD). Here, we review recent literature describing the role of glia cells and neuroinflammation in PD and LSDs, including Gaucher disease (GD) and neuronal ceroid lipofuscinosis (NCL), and highlight converging inflammation pathways that lead to neuron loss. Recent data indicates that lysosomal dysfunction and accumulation of storage materials can initiate the activation of glial cells, through interaction with cell surface or cytosolic pattern recognition receptors that detect pathogenic aggregates of cellular debris. Activated glia cells could act to protect neurons through the elimination of toxic protein or lipid aggregates early in the disease process. However prolonged glial activation that occurs over several decades in chronic-age related neurodegeneration could induce the inappropriate elimination of synapses, leading to neuron loss. These studies provide mechanistic insight into the relationship between lysosomal dysfunction and glial activation, and offer novel therapeutic pathways for the treatment of PD and LSDs focused on reducing neuroinflammation and mitigating cell loss.

Indexed as

AnimalsGaucher DiseaseHumansLysosomesNeuroinflammatory DiseasesNeuronal Ceroid-LipofuscinosesParkinson DiseaseBatten’s diseaseGaucher diseaseLysosomal storage disordersNeuroinflammationParkinson’s disease

Identifiers

PMID35063468
PMCPMC9126024
OpenAlexW4205309404

What OpenQuestion holds

Textmetadata
LicenceTDM
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 OpenQuestion graph.