Positron emission tomography after fetal transplantation in Huntington's disease | Zendy

Furtado Sarah | Zendy; Sossi Vesna | Zendy; Hauser Roberta A. | Zendy; Samii Ali | Zendy; Schulzer Michael | Zendy; Murphy Colleen B. | Zendy; Freeman Thomas B. | Zendy; Stoessl A. Jon | Zendy

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Positron emission tomography after fetal transplantation in Huntington's disease

Author(s) -

Furtado Sarah,

Sossi Vesna,

Hauser Roberta A.,

Samii Ali,

Schulzer Michael,

Murphy Colleen B.,

Freeman Thomas B.,

Stoessl A. Jon

Publication year - 2005

Publication title -

annals of neurology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 4.764

H-Index - 296

eISSN - 1531-8249

pISSN - 0364-5134

DOI - 10.1002/ana.20564

Subject(s) - positron emission tomography , transplantation , medicine , huntington's disease , fetal tissue transplantation , striatum , fetus , disease , dopamine , oncology , nuclear medicine , biology , pregnancy , genetics

H untington's disease (HD) is a progressive disorder with no known cure. We report two‐year postoperative positron emission tomography (PET) data from 7 HD patients who underwent intrastriatal fetal transplantation. Patients showed widespread reductions in glucose uptake with no significant change over 2 years. Dopamine receptor binding was significantly reduced in HD striatum. D1 binding did not change significantly following transplantation, but there was a significant loss of D2 binding. These findings may reflect loss of graft viability and/or disease progression. There was no significant relationship between changes in PET and clinical function. In summary, there was no benefit from transplantation. Ann Neurol 2005;58:331–337

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