ReviewBrain research2012
Progranulin: an emerging target for FTLD therapies.
Review in Brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.
- Association of progranulin polymorphism rs5848 with neurodegenerative diseases: a meta-analysis.Journal of neurology · 2015Pooled it
- Targeting Granulin Haploinsufficiency in Frontotemporal Dementia: From Genetic Mechanisms to Therapeutics.International journal of molecular sciences · 2025Review
- Epigenetic modulation through BET bromodomain inhibitors as a novel therapeutic strategy for progranulin-deficient frontotemporal dementia.Scientific reports · 2024Article
- Therapies for Tau-associated neurodegenerative disorders: targeting molecules, synapses, and cells.Neural regeneration research · 2023Article
- Frontotemporal-TDP and LATE Neurocognitive Disorders: A Pathophysiological and Genetic Approach.Brain sciences · 2023Review
- From basic research to the clinic: innovative therapies for ALS and FTD in the pipeline.Molecular neurodegeneration · 2020Review
- Progranulin mutations result in impaired processing of prosaposin and reduced glucocerebrosidase activity.Human molecular genetics · 2020Article
- Secreted Chaperones in Neurodegeneration.Frontiers in aging neuroscience · 2020Review
- Granulin in Frontotemporal Lobar Degeneration: Molecular Mechanisms of the Disease.Frontiers in neuroscience · 2019Article
- The role of progranulin (PGRN) in the modulation of anti-inflammatory response in asthma.Central-European journal of immunology · 2019Review
- Longitudinal structural gray matter and white matter MRI changes in presymptomatic progranulin mutation carriers.NeuroImage. Clinical · 2018Article
- The lysosomal protein cathepsin L is a progranulin protease.Molecular neurodegeneration · 2017Article
- Selectivity and Kinetic Requirements of HDAC Inhibitors as Progranulin Enhancers for Treating Frontotemporal Dementia.Cell chemical biology · 2017Article
- Frontotemporal Lobar Degeneration: Mechanisms and Therapeutic Strategies.Molecular neurobiology · 2016Review
- Molecular Pathways Bridging Frontotemporal Lobar Degeneration and Psychiatric Disorders.Frontiers in aging neuroscience · 2016Review
- FTD and ALS--translating mouse studies into clinical trials.Nature reviews. Neurology · 2015Review
- Progranulin deficiency promotes post-ischemic blood-brain barrier disruption.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Progranulin: at the interface of neurodegenerative and metabolic diseases.Trends in endocrinology and metabolism: TEM · 2013Review
- Synthetic nucleic acids delivered by exosomes: a potential therapeutic for generelated metabolic brain diseases.Metabolic brain disease · 2013Review
- Anterior brain glucose hypometabolism predates dementia in progranulin mutation carriers.Neurology · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Frontotemporal lobar degeneration (FTLD), a neurodegenerative disease primarily affecting the frontal and temporal lobes, is one of the most common types of dementia. While the majority of FTLD cases are sporadic, approximately 10-40% of patients have an inherited form of FTLD. Mutations in the progranulin gene (GRN) have recently been identified as a major cause of FTLD with ubiquitin positive inclusions (FTLD-U). Because over 70 disease-linked GRN mutations cause abnormal deficiencies in the production of PGRN, a protein that plays a crucial role in embryogenesis, cell growth and survival, wound repair and inflammation, researchers now aim to design therapies that would increase PGRN levels in affected individuals, thereby alleviating the symptoms associated with disease. Several compounds and genetic factors, as well as PGRN receptors, have recently been identified because of their ability to regulate PGRN levels. Strict quality control measures are needed given that extreme PGRN levels at either end of the spectrum - too low or too high - can lead to neurodegeneration or cancer, respectively. The aim of this review is to highlight what is known regarding PGRN biology; to improve understanding of the mechanisms involved in regulating PGRN levels and highlight studies that are laying the groundwork for the development of effective therapeutic modulators of PGRN. This article is part of a Special Issue entitled RNA-Binding Proteins.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.