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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Ghetti, Bernardino Goate, Alison Martins, Ralph N. Klunk, William E. Fox, Nick C. Aisen, Paul S. Mcdade, Eric Holtzman, David M. Xiong, Chengjie Mayeux, Richard Buckles, Virginia Cairns, Nigel J. Salloway, Stephen Blazey, Tyler M. Moulder, Krista Sperling, Reisa A. Masters, Colin L. Santacruz, Anna Rossor, Martin N. Benzinger, Tammie L. S. Bateman, Randall J. Xie, Xianyun Morris, John C. Marcus, Daniel S. Fagan, Anne M. Ringman, John M. Schofield, Peter R. Oliver, Angela |
| Organization | Dominantly Inherited Alzheimer Network |
| Description | Author Affiliation: Bateman RJ ( Washington University School of Medicine, Department of Neurology, 660 S. Euclid Ave., Box 8111, St. Louis, MO 63110, USA. batemanr@wustl.edu) |
| Abstract | BACKGROUND: The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the disease develops over many years. Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. METHODS: In this prospective, longitudinal study, we analyzed data from 128 participants who underwent baseline clinical and cognitive assessments, brain imaging, and cerebrospinal fluid (CSF) and blood tests. We used the participant's age at baseline assessment and the parent's age at the onset of symptoms of Alzheimer's disease to calculate the estimated years from expected symptom onset (age of the participant minus parent's age at symptom onset). We conducted cross-sectional analyses of baseline data in relation to estimated years from expected symptom onset in order to determine the relative order and magnitude of pathophysiological changes. RESULTS: Concentrations of amyloid-beta (Aß)(42) in the CSF appeared to decline 25 years before expected symptom onset. Aß deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset. Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset. Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset. Global cognitive impairment, as measured by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset, and patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset. CONCLUSIONS: We found that autosomal dominant Alzheimer's disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment. Our results require confirmation with the use of longitudinal data and may not apply to patients with sporadic Alzheimer's disease. (Funded by the National Institute on Aging and others; DIAN ClinicalTrials.gov number, NCT00869817.). |
| ISSN | 00284793 |
| e-ISSN | 15334406 |
| Journal | New England Journal of Medicine |
| Issue Number | 9 |
| Volume Number | 367 |
| Language | English |
| Publisher | Massachusetts Medical Society (United States) |
| Publisher Date | 2012-08-30 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Alzheimer Disease Metabolism Amyloid Beta-Peptides Cerebrospinal Fluid Age Of Onset Genetics Psychology Biological Markers Brain Pathology Cross-Sectional Studies Genes, Dominant Glucose Longitudinal Studies Magnetic Resonance Imaging Mutation Neuropsychological Tests Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Medicine |
| Content Type | Text |
| Resource Type | Article |
| Subject | Medicine |
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