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 Michael W. Weiner
Total Records ( 8 ) for Michael W. Weiner
  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.
  Zaven S. Khachaturian , Ronald C. Petersen , Peter J. Snyder , Ara S. Khachaturian , Paul Aisen , Mony de Leon , Barry D. Greenberg , Walter Kukull , Paul Maruff , Reisa A. Sperling , Yaakov Stern , Jacques Touchon , Bruno Vellas , Sandrine Andrieu , Michael W. Weiner , Maria C. Carrillo and Lisa J. Bain
  The fourth Leon Thal Symposium (LTS2010) was convened in Toulouse, France, on November 3, 2010. This symposium reviewed design parameters that are necessary to develop comprehensive national databases on healthy aging. Such datasets offer the potential to serve as the foundation for a systems-approach to solve the dual public health problems of: (1) early detection of people who are at elevated risk for Alzheimer‘s disease, and (2) the development of interventions to delay onset of, or prevent, late-life dementia. The symposium considered three interrelated components of a National Database for Longitudinal Studies on Healthy Aging as follows: (a) a registry of healthy aging adults; (b) refined computer-based assessments for data gathering, including assessments of behavioral/memory changes associated with aging that are appropriate for broad use in nonexpert settings; and (c) high performance computing/supercomputer-based approaches for health data modeling and mining
  Stephen D. Weigand , Prashanthi Vemuri , Heather J. Wiste , Matthew L. Senjem , Vernon S. Pankratz , Paul S. Aisen , Michael W. Weiner , Ronald C. Petersen , Leslie M. Shaw , John Q. Trojanowski , David S. Knopman and Clifford R. Jack
  Background Positron-emission tomography (PET) imaging of amyloid with Pittsburgh Compound B (PIB) and Aβ42 levels in the cerebrospinal fluid (CSF Aβ42) demonstrate a highly significant inverse correlation. Both these techniques are presumed to measure brain Aβ amyloid load. The objectives of this study were to develop a method to transform CSF Aβ42 measures into calculated PIB measures (PIBcalc) of Aβ amyloid load, and to partially validate the method in an independent sample of subjects. Methods In all, 41 subjects from the Alzheimer‘s Disease Neuroimaging Initiative (ADNI) underwent PIB PET imaging and lumbar puncture (LP) at the same time. This sample, referred to as the ”training“ sample (nine cognitively normal subjects, 22 subjects with mild cognitive impairment, and 10 subjects with Alzheimer‘s disease), was used to develop a regression model by which CSF Aβ42 (with apolipoprotein E ɛ4 carrier status as a covariate) was transformed into units of PIB PET (PIBcalc). An independent ”supporting“ sample of 362 ADNI subjects (105 cognitively normal subjects, 164 subjects with mild cognitive impairment, and 93 subjects with Alzheime‘s disease) who underwent LP but not PIB PET imaging had their CSF Aβ42 values converted to PIBcalc. These values were compared with the overall PIB PET distribution found in the ADNI subjects (n = 102). Results A linear regression model demonstrates good prediction of actual PIB PET from CSF Aβ42 measures obtained in the training sample (R2 = 0.77, P < .001). PIBcalc data (derived from CSF Aβ42) in the supporting sample of 362 ADNI subjects who underwent LP but not PIB PET imaging demonstrate group-wise distributions that are highly consistent with the larger ADNI PIB PET distribution and with published PIB PET imaging studies. Conclusion Although the precise parameters of this model are specific for the ADNI sample, we conclude that CSF Aβ42 can be transformed into PIBcalc measures of Aβ amyloid load. Brain Aβ amyloid load can be ascertained at baseline in therapeutic or observational studies by either CSF or amyloid PET imaging and the data can be pooled using well-established multiple imputation techniques that account for the uncertainty in a CSF-based PIBcalc value.
  Michael W. Weiner , Carl Sadowsky , Judith Saxton , Robert K. Hofbauer , Stephen M. Graham , ung Yun Yu , Shaoyi Li , Hai-An Hsu , Joyce Suhy , Moshe Fridman and James L. Perhach
  Background This study was designed to assess changes in brain volume and cognitive abilities in memantine-treated patients with Alzheimer‘s disease (AD) by using an exploratory, single-arm, delayed-start design. Methods Cholinesterase inhibitor-treated patients with AD (N = 47; Mini-Mental State Examination score range: 15–23) were enrolled in an observational lead-in period (weeks: 1–24), followed by an open-label period of add-on memantine treatment (weeks: 25–48). The patients underwent magnetic resonance imaging at weeks 0 (baseline), 24 (immediately before memantine initiation), and 48 (endpoint), and a battery of neuropsychological tests at weeks 0, 24, 28, 36, and 48. The primary outcome measure was the annualized rate of change (%) in total brain volume (TBV) between the two study periods. Data were analyzed using paired t-tests. Results There were no statistically significant differences in the rates of change in TBV, ventricular volume, or left hippocampal volume between the study periods; however, the memantine treatment period was associated with a significantly slower right hippocampal atrophy (−5.5% ± 12.0% vs −10.8% ± 7.2%; P = .038). Memantine treatment was also associated with superior performances on the Boston Naming Test (P = .034) and the Trail Making Test, Part B (P = .001), but also with a higher number of errors (i.e., repetitions and intrusions) on the California Verbal Learning Test. Memantine was found to be safe and well tolerated. Conclusions In this study, no difference in the rates of TBV change between the two periods was observed; however, memantine treatment was found to be associated with slowing of right hippocampal atrophy, and with improvement on one test of executive functioning as well as a test of confrontation naming ability. Trials using structural magnetic resonance imaging and a delayed-start design may be a feasible option for the assessment of treatments for AD.
  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.
  Maria C. Carrillo , Lisa J. Bain , Giovanni B. Frisoni and Michael W. Weiner
  The Alzheimer‘s Disease Neuroimaging Initiative (ADNI) was launched in 2003 to speed drug development by validating imaging and blood/cerebrospinal fluid biomarkers for Alzheimer‘s disease clinical treatment trials. ADNI is a naturalistic (nontreatment) multisite longitudinal study. A true public–private partnership, the first phase of ADNI (ADNI 1) set a new standard for data sharing without embargo. In addition, it has been extended to 2017 by additional funding (North American-ADNI Grand Opportunities and ADNI 2) as well as multiple projects around the world, collectively known as Worldwide ADNI (WW-ADNI). The goal of WW-ADNI is to harmonize projects and results across different geographical sites and to encourage and harmonize data management and availability to investigators around the world. WW-ADNI projects are currently underway in North America, Europe, Japan, Australia, Korea, Taiwan, and Argentina, with a nascent program in China and a possible future program in Brazil.
  Jon B. Toledo , Estefania Toledo , Michael W. Weiner , Clifford R. Jack , William Jagust , Virginia M.-Y. Lee , Leslie M. Shaw and John Q. Trojanowski
  Background There is epidemiological evidence that cardiovascular risk factors (CVRF) also are risk factors for Alzheimer‘s disease, but there is limited information on this from neuropathological studies, and even less from in vivo studies. Therefore, we examined the relationship between CVRF and amyloid-β (Aβ) brain burden measured by Pittsburgh Compound B-positron emission tomography (PiB-PET) studies in the Alzheimer‘s Disease Neuroimaging Initiative. Methods Ninety-nine subjects from the Alzheimer‘s Disease Neuroimaging Initiative cohort who had a PiB-PET study measure, apolipoprotein E genotyping data, and information available on CVRF (body mass index [BMI], systolic blood pressure, diastolic blood pressure [DBP], and cholesterol and fasting glucose test results) were included. Eighty-one subjects also had plasma cortisol, C-reactive protein, and superoxide dismutase 1 measurements. Stepwise regression models were used to assess the relation between the CVRF and the composite PiB-PET score. Results The first model included the following as baseline variables: age, clinical diagnosis, number of apolipoprotein ɛ4 alleles, BMI (P = .023), and DBP (P = .012). BMI showed an inverse relation with PiB-PET score, and DBP had a positive relation with PiB-PET score. In the second adjusted model, cortisol plasma levels were also associated with PiB-PET score (P = .004). Systolic blood pressure, cholesterol, or impaired fasting glucose were not found to be associated with PiB-PET values. Conclusion In this cross-sectional study, we found an association between Aβ brain burden measured in vivo and DBP and cortisol, indicating a possible link between these CVRF and Aβ burden measured by PiB-PET. These findings highlight the utility of biomarkers to explore potential pathways linking diverse Alzheimer‘s disease risk factors.
  Timothy C. Durazzo , Philip S. Insel and Michael W. Weiner
  Background Little is known about the effects of cigarette smoking on longitudinal brain morphological changes in the elderly. This study investigated the effects of a history of cigarette smoking on changes in regional brain volumes over 2 years in healthy, cognitively intact elderly individuals. We predicted that individuals with a history of cigarette smoking, compared with never smokers, demonstrate greater rate of atrophy over 2 years in regions that manifest morphological abnormalities in the early stages of Alzheimer‘s disease (AD), as well as in the extended brain reward/executive oversight system (BREOS), which is implicated in the development and maintenance of substance use disorders. Methods Participants were healthy, cognitively normal elderly control subjects (75.9 ± 4.8 years of age) with any lifetime history of cigarette smoking (n = 68) or no history of smoking (n = 118). Data were obtained through the Alzheimer Disease Neuroimaging Initiative from 2005 to 2010. Participants completed four magnetic resonance scans over 2 years. A standardized protocol using high-resolution three-dimensional T1-weighted sequences at 1.5 T was used for structural imaging and regional brain volumetric analyses. Results Smokers demonstrated a significantly greater atrophy rate over 2 years than nonsmokers in multiple brain regions associated with the early stages of AD, as well as in the BREOS system. Groups did not differ on the rate of global cortical atrophy. Conclusions A history of cigarette smoking in this healthy elderly cohort was associated with decreased structural integrity of multiple brain regions, which manifested as a greater rate of atrophy over 2 years in regions specifically affected by incipient AD as well as chronic substance abuse.
Copyright   |   Desclaimer   |    Privacy Policy   |   Browsers   |   Accessibility