Evidence map›Paper›PMID 31962288›Full record

ReviewNeuropharmacology2020

Approaches to develop therapeutics to treat frontotemporal dementia.

Lisa P Elia, Terry Reisine, Amela Alijagic, Steven Finkbeiner

Open access · greenAbstract readReview
In one paragraph

Review in Neuropharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-weighted citation impact, top 26% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. TRAP1 and its therapeutic potential.Bioorganic & medicinal chemistry letters · 2025
    Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Histone Modifications in Neurological Disorders.Advances in experimental medicine and biology · 2022
    Review
  9. Article
  10. Anti-sortilin1 Antibody Up-Regulates ProgranulinFrontiers in neuroscience · 2020
    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

4 authors at 2 institutions in 1 country.

Lisa P EliaCenter for Systems and Therapeutics and Taube/Koret Center for Neurodegenerative Disease Research, San Francisco, CA, USA; The J. David Gladstone Institutes, San Francisco, CA, USA. Electronic address: lisa.elia@gladstone.ucsf.edu.
Terry ReisineIndependent Scientific Consultant, Santa Cruz, CA, USA.
Amela AlijagicCenter for Systems and Therapeutics and Taube/Koret Center for Neurodegenerative Disease Research, San Francisco, CA, USA; The J. David Gladstone Institutes, San Francisco, CA, USA.
Steven FinkbeinerCenter for Systems and Therapeutics and Taube/Koret Center for Neurodegenerative Disease Research, San Francisco, CA, USA; The J. David Gladstone Institutes, San Francisco, CA, USA; Departments of Neurology and Physiology, UCSF, San Francisco, CA, USA. Electronic address: steve.finkbeiner@gladstone.ucsf.edu.
Taube Koret Center · USGladstone Institutes · US

Funding

The proteasome in aging and neurodegenerative diseaseP01AG054407 · NIA · NORTHWESTERN UNIVERSITY · PI FRYDMAN, JUDITH · 2018 to 2022
$14.0M
Dysfunction of the Autophagy-Lysosomal Pathway as a Common Mechanism of NeurodegenerationRF1AG058476 · NIA · J. DAVID GLADSTONE INSTITUTES · PI FINKBEINER, STEVEN M · 2017 to 2018
$4.1M
EXTRAMULAR RESEARCH FACILITIES CONSTRUCTIONC06RR018928 · NCRR · J. DAVID GLADSTONE INSTITUTES · PI MAHLEY, ROBERT W. · 2003 to 2003
$2.1M
TRAP1 and FOXO1 as modifiers of progranulin and FTLDR21NS093236 · NINDS · J. DAVID GLADSTONE INSTITUTES · PI FINKBEINER, STEVEN M · 2016 to 2017
$521k
NCRR NIH HHS C06 RR018928NIA NIH HHS P01 AG054407NIA NIH HHS RF1 AG058476NINDS NIH HHS R21 NS093236
6 · The paper itself

Abstract

Frontotemporal degeneration (FTD) is a complex disease presenting as a spectrum of clinical disorders with progressive degeneration of frontal and temporal brain cortices and extensive neuroinflammation that result in personality and behavior changes, and eventually, death. There are currently no effective therapies for FTD. While 60-70% of FTD patients are sporadic cases, the other 30-40% are heritable (familial) cases linked to mutations in several known genes. We focus here on FTD caused by mutations in the GRN gene, which encodes a secreted protein, progranulin (PGRN), that has diverse roles in regulating cell survival, immune responses, and autophagy and lysosome function in the brain. FTD-linked mutations in GRN reduce brain PGRN levels that lead to autophagy and lysosome dysfunction, TDP43 accumulation, excessive microglial activation, astrogliosis, and neuron death through still poorly understood mechanisms. PGRN insufficiency has also been linked to Alzheimer's disease (AD), and so the development of therapeutics for GRN-linked FTD that restore PGRN levels and function may have broader application for other neurodegenerative diseases. This review focuses on a strategy to increase PGRN to functional, healthy levels in the brain by identifying novel genetic and chemical modulators of neuronal PGRN levels. This article is part of the special issue entitled 'The Quest for Disease-Modifying Therapies for Neurodegenerative Disorders'.

Indexed as

AnimalsFrontal LobeFrontotemporal DementiaGenetic TherapyHSP90 Heat-Shock ProteinsHumansProgranulinsQuinolonesTemporal LobeTyrosine5-amino-7-(cyclohexylamino)-1-ethyl-6-fluoro-4-oxo-1,4-dihydroquinoline-3-carboxylic acidHSP90 Heat-Shock ProteinsProgranulinspsammaplysene AQuinolonesTRAP1 protein, humanTyrosineADFTDLysosomeNeurodegenerativeProgranulinTherapeutics

Identifiers

PMID31962288
PMCPMC8101984
OpenAlexW3000520496

What Socratic 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 Socratic graph.