Evidence map›Paper›PMID 11106399›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2000

Transplanted fetal striatum in Huntington's disease: phenotypic development and lack of pathology.

T B Freeman, F Cicchetti, R A Hauser, T W Deacon, X J Li, S M Hersch, G M Nauert, P R Sanberg, J H Kordower, S Saporta and 1 more

Abstract readCase Reports
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

54 citing papers in PubMed, 262 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Advancements in surgical treatments for Huntington disease: From pallidotomy to experimental therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Restorative Strategies in Movement Disorders: the Contribution of Imaging.Current neurology and neuroscience reports · 2017
    Review
  16. Article
  17. Review
  18. Review
  19. Review
  20. Novel targets for Huntington's disease: future prospects.Degenerative neurological and neuromuscular disease · 2016
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

T B FreemanDepartment of Neurosurgery, Department of Pharmacology and Experimental Therapeutics, and The Neuroscience Program, University of South Florida, Tampa, FL 33606, USA. tfreeman@com1.med.usf.edu
F Cicchetti
R A Hauser
T W Deacon
X J Li
S M Hersch
G M Nauert
P R Sanberg
J H Kordower
S Saporta
O Isacson
University of South Florida · USMcLean Hospital · US

Funding

TRANSGENIC XENOTRANSPLANTS FOR HUNTINGTON'S DISEASER01NS030064 · NINDS · MC LEAN HOSPITAL (BELMONT, MA) · PI ISACSON, OLE · 1992 to 2002
$1.1M
NINDS NIH HHS NS-30064NINDS NIH HHS R01 NS030064
6 · The paper itself

Abstract

Neural and stem cell transplantation is emerging as a potential treatment for neurodegenerative diseases. Transplantation of specific committed neuroblasts (fetal neurons) to the adult brain provides such scientific exploration of these new potential therapies. Huntington's disease (HD) is a fatal, incurable autosomal dominant (CAG repeat expansion of huntingtin protein) neurodegenerative disorder with primary neuronal pathology within the caudate-putamen (striatum). In a clinical trial of human fetal striatal tissue transplantation, one patient died 18 months after transplantation from cardiovascular disease, and postmortem histological analysis demonstrated surviving transplanted cells with typical morphology of the developing striatum. Selective markers of both striatal projection and interneurons such as dopamine and c-AMP-related phosphoprotein, calretinin, acetylcholinesterase, choline acetyltransferase, tyrosine hydroxylase, calbindin, enkephalin, and substance P showed positive transplant regions clearly innervated by host tyrosine hydroxylase fibers. There was no histological evidence of immune rejection including microglia and macrophages. Notably, neuronal protein aggregates of mutated huntingtin, which is typical HD neuropathology, were not found within the transplanted fetal tissue. Thus, although there is a genetically predetermined process causing neuronal death within the HD striatum, implanted fetal neural cells lacking the mutant HD gene may be able to replace damaged host neurons and reconstitute damaged neuronal connections. This study demonstrates that grafts derived from human fetal striatal tissue can survive, develop, and are unaffected by the disease process, at least for 18 months, after transplantation into a patient with HD.

Indexed as

Fetal Tissue TransplantationCorpus StriatumHumansHuntington DiseaseImmunohistochemistryMaleMiddle AgedPhenotype

Identifiers

PMID11106399
PMCPMC17669
OpenAlexW2101326888

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.