Evidence map›Paper›PMID 19166904›Full record

ReviewBiochimica et biophysica acta2009

Amyloid precursor protein and alpha synuclein translation, implications for iron and inflammation in neurodegenerative diseases.

Catherine M Cahill, Debomoy K Lahiri, Xudong Huang, Jack T Rogers

Abstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

69 citing papers in PubMed, 103 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. FeInternational journal of molecular sciences · 2025
    Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Iron imbalance in neurodegeneration.Molecular psychiatry · 2024
    Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

9 more citing papers are in PubMed but not listed here.

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 3 institutions in 1 country.

Catherine M CahillNeurochemistry Laboratory, Department of Psychiatry-Neuroscience, Massachusetts General Hospital (East), Harvard Medical School, CNY2, Building 149, Charlestown, MA 02129, USA.
Debomoy K Lahiri
Xudong Huang
Jack T Rogers
Harvard University · USBrigham and Women's Hospital · USIndiana University School of Medicine

Funding

MLSN Screen of the PD Alpha Synuclein 5'UTRR21NS059434 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ROGERS, JACK T · 2007 to 2008
$263k
NIA NIH HHS AG02081NINDS NIH HHS R21 NS059434
6 · The paper itself

Abstract

Recent studies that alleles in the hemochromatosis gene may accelerate the onset of Alzheimer's disease by five years have validated interest in the model in which metals (particularly iron) accelerate disease course. Biochemical and biophysical measurements demonstrated the presence of elevated levels of neurotoxic copper zinc and iron in the brains of AD patients. Intracellular levels of APP holoprotein were shown to be modulated by iron by a mechanism that is similar to the translation control of the ferritin L- and H mRNAs by iron-responsive element (IRE) RNA stem loops in their 5' untranslated regions (5'UTRs). More recently a putative IRE-like sequence was hypothesized present in the Parkinsons's alpha synuclein (ASYN) transcript (see [A.L. Friedlich, R.E. Tanzi, J.T. Rogers, The 5'-untranslated region of Parkinson's disease alpha-synuclein messenger RNA contains a predicted iron responsive element, Mol. Psychiatry 12 (2007) 222-223. [6]]). Together with the demonstration of metal dependent translation of APP mRNA, the involvement of metals in the plaque of AD patients and of increased iron in striatal neurons in the substantia nigra (SN) of Parkinson's disease patients have stimulated the development of metal attenuating agents and iron chelators as a major new therapeutic strategy for the treatment of these neurodegenerative diseases. In the case of AD, metal based therapeutics may ultimately prove more cost effective than the use of an amyloid vaccine as the preferred anti-amyloid therapeutic strategy to ameliorate the cognitive decline of AD patients.

Indexed as

alpha-SynucleinAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsBase SequenceChelating AgentsFerritinsHomeostasisHumansInflammationIronMolecular Sequence DataNeurodegenerative DiseasesParkinson DiseaseProtein BiosynthesisReceptors, Transferrinalpha-SynucleinAmyloid beta-Protein PrecursorChelating AgentsFerritinsIronReceptors, TransferrinRNA, Messengertau Proteins

Identifiers

PMID19166904
PMCPMC3981543
OpenAlexW1975559668

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.