Asian Science Citation Index is committed to provide an authoritative, trusted and significant information by the coverage of the most important and influential journals to meet the needs of the global scientific community.  
ASCI Database
308-Lasani Town,
Sargodha Road,
Faisalabad, Pakistan
Fax: +92-41-8815544
Contact Via Web
Suggest a Journal
Articles by William J. Jagust
Total Records ( 2 ) for William J. Jagust
  Norbert Schuff , Shinji Matsumoto , Joseph Kmiecik , Colin Studholme , Antao Du , Frank Ezekiel , Bruce L. Miller , Joel H. Kramer , William J. Jagust , Helen C. Chui and Michael W. Weiner
  Background Our objectives were to compare the effects of subcortical ischemic vascular dementia (SIVD) and Alzheimer's disease (AD) on cerebral blood flow (CBF), and then to analyze the relationship between CBF and subcortical vascular disease, measured as volume of white-matter lesions (WMLs). Methods Eight mildly demented patients with SIVD (mean ± SD; aged 77 ± 8 years; Mini-Mental State Examination score 26 ± 3 years) and 14 patients with AD were compared with 18 cognitively normal elderly subjects. All subjects had CBF measured using arterial spin-labeling magnetic resonance imaging, and brain volumes were assessed using structural magnetic resonance imaging. Results AD and SIVD showed marked CBF reductions in the frontal (P = 0.001) and parietal (P = 0.001) cortices. In SIVD, increased subcortical WMLs were associated with reduced CBF in the frontal cortex (P = 0.04), in addition to cortical atrophy (frontal, P = 0.05; parietal, P = 0.03). Conclusions Subcortical vascular disease is associated with reduced CBF in the cortex, irrespective of brain atrophy.
  Gloria C. Chiang , Philip S. Insel , Duygu Tosun , Norbert Schuff , Diana Truran- Sacrey , Sky T. Raptentsetsang , Paul M. Thompson , Eric M. Reiman , Clifford R. Jack , Nick C. Fox , William J. Jagust , Danielle J. Harvey , Laurel A. Beckett , Anthony Gamst , Paul S. Aisen , Ron C. Petersen and Michael W. Weiner
  Background The majority of studies relating amyloid pathology with brain volumes have been cross-sectional. Apolipoprotein ɛ4 (APOE ɛ4), a genetic risk factor for Alzheimer‘s disease, is also known to be associated with hippocampal volume loss. No studies have considered the effects of amyloid pathology and APOE ɛ4 together on longitudinal volume loss. Methods We evaluated whether an abnormal level of cerebrospinal fluid beta-amyloid (CSF Aβ) and APOE ɛ4 carrier status were independently associated with greater hippocampal volume loss over 1 year. We then assessed whether APOE ɛ4 status and CSF Aβ acted synergistically, testing the significance of an interaction term in the regression analysis. We included 297 participants: 77 cognitively normal, 144 with mild cognitive impairment (MCI), and 76 with Alzheimer‘s disease. Results An abnormal CSF Aβ level was found to be associated with greater hippocampal volume loss over 1 year in each group. APOE ɛ4 was associated with hippocampal volume loss only in the cognitively normal and MCI groups. APOE ɛ4 carriers with abnormal CSF Aβ in the MCI group acted synergistically to produce disproportionately greater volume loss than noncarriers. Conclusion Baseline CSF Aβ predicts progression of hippocampal volume loss. APOE ɛ4 carrier status amplifies the degree of neurodegeneration in MCI. Understanding the effect of interactions between genetic risk and amyloid pathology will be important in clinical trials and our understanding of the disease process.
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility