This Article  • Full text  • PDF  • CME Course for This Article  • Reply to article  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Citing articles on HighWire  • Citing articles on Web of Science (1)  • Contact me when this article is cited  Related Content  • Related articles  • Similar articles in this journal  Topic Collections  • Alzheimer Disease  • Cognitive Disorders  • Neurology, Other  • Alert me on articles by topic  Social Bookmarking   What's this?

Ville Leinonen, MD, PhD; Irina Alafuzoff, MD, PhD; Sargo Aalto, MSc; Timo Suotunen, BM; Sakari Savolainen, MD, PhD; Kjell Någren, PhD; Tero Tapiola, MD, PhD; Tuula Pirttilä, MD, PhD; Jaakko Rinne, MD, PhD; Juha E. Jääskeläinen, MD, PhD; Hilkka Soininen, MD, PhD; Juha O. Rinne, MD, PhD

Arch Neurol. 2008;65(10):1304-1309.

Objective  To compare carbon 11–labeled Pittsburgh Compound B ([¹¹C]PiB) positron emission tomography (PET) findings in patients with and without Alzheimer disease lesions in frontal cortical biopsy specimens.

Design  Cross-sectional study of [¹¹C]PiB PET findings in patients with or without β-amyloid (Aβ) aggregates in frontal cortical biopsy specimens.

Setting  Two university hospitals in Finland.

Patients  Ten patients who had undergone intraventricular pressure monitoring with a frontal cortical biopsy (evaluated for Aβ aggregates and hyperphosphorylated tau) for suspected normal-pressure hydrocephalus.

Interventions  [¹¹C]PiB PET and evaluation for cognitive impairment using a battery of neuropsychological tests.

Main Outcome Measures  Immunohistochemical evaluation for Aβ aggregates and hyperphosphorylated tau in the frontal cortical biopsy specimen and [¹¹C]PiB PET.

Results  In patients with Aβ aggregates in the frontal cortical biopsy specimen, PET imaging revealed higher [¹¹C]PiB uptake (P < .05) in the frontal, parietal, and lateral temporal cortices and in the striatum as compared with the patients without frontal Aβ deposits.

Conclusions  Our study supports the use of noninvasive [¹¹C]PiB PET in the assessment of Aβ deposition in the brain. Large prospective studies are required to verify whether [¹¹C]PiB PET will be a diagnostic aid, particularly in early Alzheimer disease.

Author Affiliations: Departments of Neurosurgery (Drs Leinonen, Savolainen, J. Rinne, and Jääskeläinen) and Neurology (Drs Tapiola, Pirttilä, and Soininen), Kuopio University Hospital and Unit of Pathology and Neurology, Department of Clinical Medicine (Dr Alafuzoff), and Unit of Neurology, Institute of Clinical Medicine (Drs Pirttilä and Soininen), University of Kuopio, Kuopio and Turku PET Centre, University of Turku, Turku (Drs Någren and J. O. Rinne and Messrs Aalto and Suotunen), Finland.

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?

RELATED ARTICLES

This Month in Archives of Neurology
Arch Neurol. 2008;65(10):1278-1280.
FULL TEXT  

Biopsy Support for the Validity of Pittsburgh Compound B Positron Emission Tomography With a Twist
William E. Klunk
Arch Neurol. 2008;65(10):1281-1283.
EXTRACT | FULL TEXT  

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

11C-PiB PET studies in typical sporadic Creutzfeldt-Jakob disease
Villemagne et al.
J. Neurol. Neurosurg. Psychiatry 2009;80:998-1001.
ABSTRACT | FULL TEXT  

Phase 1 Study of the Pittsburgh Compound B Derivative 18F-Flutemetamol in Healthy Volunteers and Patients with Probable Alzheimer Disease
Nelissen et al.
JNM 2009;50:1251-1259.
ABSTRACT | FULL TEXT  

Serial PIB and MRI in normal, mild cognitive impairment and Alzheimer's disease: implications for sequence of pathological events in Alzheimer's disease
Jack et al.
Brain 2009;132:1355-1365.
ABSTRACT | FULL TEXT  

Biopsy Support for the Validity of Pittsburgh Compound B Positron Emission Tomography With a Twist
Klunk
Arch Neurol 2008;65:1281-1283.
FULL TEXT