Evidence map›Paper›PMID 22112803›Full record

ReviewMolecular neurodegeneration2011

Transthyretin and the brain re-visited: is neuronal synthesis of transthyretin protective in Alzheimer's disease?

Xinyi Li, Joel N Buxbaum

Open access · goldAbstract readReview
In one paragraph

Review in Molecular neurodegeneration, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

60 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
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  6. Article
  7. Article
  8. Primary Hypothyroidism and Alzheimer's Disease: A Tale of Two.Cellular and molecular neurobiology · 2023
    Review
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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

2 authors at 1 institution in 1 country.

Xinyi LiDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Rd,, MEM-230, La Jolla, CA 92037, USA.
Joel N Buxbaum
Scripps Research Institute · US

Funding

VIRUS-INDUCED BRAIN PATHOLOGYP50AG005131 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BREWER, JAMES B · 1985 to 2018
$55.4M
Tissue Culture CoreP01AG022074 · NIA · J. DAVID GLADSTONE INSTITUTES · PI MASLIAH, ELIEZER · 2003 to 2012
$27.0M
Viral VectorsP01AG010435 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI TUSZYNSKI, MARK H. · 1991 to 2014
$20.9M
La Jolla Interdisciplinary Neuroscience Center Cores - Vital VP30NS057096 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI LIPTON, STUART A · 2006 to 2010
$12.7M
B-Synuclein as a Treatment for Lewy Body DiseaseR01AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI RISSMAN, ROBERT · 2001 to 2021
$5.2M
Transgenic Models to Study Alzheimer's DiseaseR37AG011385 · NIA · J. DAVID GLADSTONE INSTITUTES · PI MUCKE, LENNART · 2002 to 2011
$4.9M
TRANSGENIC MODELS TO SUDY ALZHEIMERS DISEASER01AG011385 · NIA · SCRIPPS RESEARCH INSTITUTE · PI MUCKE, LENNART · 1992 to 2017
$3.2M
a-synuclein clearance strategies for the treatment of Lewy body disease.R37AG018440 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MASLIAH, ELIEZER · 2006 to 2014
$2.7M
Aging and the Tissue Response to Misfolded ProteinsR01AG030027 · NIA · SCRIPPS RESEARCH INSTITUTE, THE · PI BUXBAUM, JOEL N · 2008 to 2012
$2.1M
NIA NIH HHS AG10435NIA NIH HHS AG11385NIA NIH HHS AG18440NIA NIH HHS AG22074NIA NIH HHS AG5131NIA NIH HHS AG R01 030027NINDS NIH HHS NS057096
6 · The paper itself

Abstract

Since the mid-1990's a trickle of publications from scattered independent laboratories have presented data suggesting that the systemic amyloid precursor transthyretin (TTR) could interact with the amyloidogenic β-amyloid (Aβ) peptide of Alzheimer's disease (AD). The notion that one amyloid precursor could actually inhibit amyloid fibril formation by another seemed quite far-fetched. Further it seemed clear that within the CNS, TTR was only produced in choroid plexus epithelial cells, not in neurons. The most enthusiastic of the authors proclaimed that TTR sequestered Aβ in vivo resulting in a lowered TTR level in the cerebrospinal fluid (CSF) of AD patients and that the relationship was salutary. More circumspect investigators merely showed in vitro interaction between the two molecules. A single in vivo study in Caenorhabditis elegans suggested that wild type human TTR could suppress the abnormalities seen when Aβ was expressed in the muscle cells of the worm. Subsequent studies in human Aβ transgenic mice, including those from our laboratory, also suggested that the interaction reduced the Aβ deposition phenotype. We have reviewed the literature analyzing the relationship including recent data examining potential mechanisms that could explain the effect. We have proposed a model which is consistent with most of the published data and current notions of AD pathogenesis and can serve as a hypothesis which can be tested.

Indexed as

AgingAlzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainDisease Models, AnimalHumansNeuronsNeuroprotective AgentsPrealbuminProtein MultimerizationAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAPP protein, humanNeuroprotective AgentsPrealbumin

Identifiers

PMID22112803
PMCPMC3267701
OpenAlexW2116622558

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.