Evidence map›Paper›PMID 38117343›Full record

ArticleNeurogenetics2024

Dem-Aging: autophagy-related pathologies and the "two faces of dementia".

N Gammaldi, S Doccini, S Bernardi, M Marchese, M Cecchini, R Ceravolo, S Rapposelli, G M Ratto, S Rocchiccioli, F Pezzini and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Neurogenetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 44% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

12 authors at 6 institutions in 1 country.

N GammaldiDepartment of Neurosciences, Psychology, Drug Research and Child Health (NEUROFARBA), University of Florence, Florence, Italy.
S DocciniMolecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy. stefano.doccini@fsm.unipi.it.
S BernardiMolecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy.
M MarcheseMolecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy.
M CecchiniNational Enterprise for nanoScience and nanoTechnology (NEST), Nanoscience Institute-National Research Council (CNR) and Scuola Normale Superiore, Pisa, Italy.
R CeravoloUnit of Neurology, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy.
S RapposelliDepartment of Pharmacy, University of Pisa, Pisa, Italy.
G M RattoNational Enterprise for nanoScience and nanoTechnology (NEST), Nanoscience Institute-National Research Council (CNR) and Scuola Normale Superiore, Pisa, Italy.
S RocchiccioliClinical Physiology-National Research Council (IFC-CNR), Pisa, Italy.
F PezziniDepartment of Surgery, Dentistry, Pediatrics and Gynecology (Child Neurology and Psychiatry), University of Verona, Verona, Italy.
F M SantorelliMolecular Medicine for Neurodegenerative and Neuromuscular Diseases Unit, IRCCS Stella Maris Foundation, Pisa, Italy.ORCID http://orcid.org/0000-0002-1359-9062
DEM-AGING Network
Fondazione Stella Maris · ITUniversity of Pisa · ITNational Enterprise for NanoScience and NanoTechnology · ITNational Research Council · ITScuola Normale Superiore · ITUniversity of Verona · IT

Funding

Ministero della Salute Ricerca Corrente
6 · The paper itself

Abstract

Neuronal ceroid lipofuscinosis (NCL) is an umbrella term referring to the most frequent childhood-onset neurodegenerative diseases, which are also the main cause of childhood dementia. Although the molecular mechanisms underlying the NCLs remain elusive, evidence is increasingly pointing to shared disease pathways and common clinical features across the disease forms. The characterization of pathological mechanisms, disease modifiers, and biomarkers might facilitate the development of treatment strategies.The DEM-AGING project aims to define molecular signatures in NCL and expedite biomarker discovery with a view to identifying novel targets for monitoring disease status and progression and accelerating clinical trial readiness in this field. In this study, we fused multiomic assessments in established NCL models with similar data on the more common late-onset neurodegenerative conditions in order to test the hypothesis of shared molecular fingerprints critical to the underlying pathological mechanisms. Our aim, ultimately, is to combine data analysis, cell models, and omic strategies in an effort to trace new routes to therapies that might readily be applied in the most common forms of dementia.

Indexed as

DementiaNeuronal Ceroid-LipofuscinosesHumansAutophagyBiomarkersDementiaNeuronal ceroid lipofuscinosis

Identifiers

PMID38117343
OpenAlexW4390005667

What OpenQuestion 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 OpenQuestion graph.