Neuroimaging Changes in Preclinical Alzheimer's Disease Alzheimer’s disease (AD) is a late-life neurodegenerative disorder that results in the insidious onset and gradual progression of cognitive impairment (Katzman, 1986). As the leading cause of dementia, AD is responsible for upwards of two-thirds of dementia cases. The prevalence of this progressive degenerative brain disorder rises in an ... Article
Article  |   December 01, 2003
Neuroimaging Changes in Preclinical Alzheimer's Disease
Author Affiliations & Notes
  • Nikki R. Horne
    San Diego State University/University of California, San Diego
    University of California, San Diego
  • Mark W. Bondi
    VA Medical Center, San Diego
Article Information
Special Populations / Older Adults & Aging / Telepractice & Computer-Based Approaches / Attention, Memory & Executive Functions / Articles
Article   |   December 01, 2003
Neuroimaging Changes in Preclinical Alzheimer's Disease
SIG 2 Perspectives on Neurophysiology and Neurogenic Speech and Language Disorders, December 2003, Vol. 13, 12-19. doi:10.1044/nnsld13.4.12
SIG 2 Perspectives on Neurophysiology and Neurogenic Speech and Language Disorders, December 2003, Vol. 13, 12-19. doi:10.1044/nnsld13.4.12
Alzheimer’s disease (AD) is a late-life neurodegenerative disorder that results in the insidious onset and gradual progression of cognitive impairment (Katzman, 1986). As the leading cause of dementia, AD is responsible for upwards of two-thirds of dementia cases. The prevalence of this progressive degenerative brain disorder rises in an exponential fashion between the ages of 65 and 85 (Kawas & Katzman, 1999). As atrophy, neuron loss, and the formation of senile plaques and neurofibrillary tangles progress, patients with AD present with a gradual decline of memory and other cognitive abilities, eventually leading to severe functional impairment and the need for total care. The slow neurodegenerative changes are ongoing for years, perhaps decades, however, before the appearance of the definitive clinical syndrome (Gómez-Isla et al., 1996). Subtle, but detectable, cognitive signs and accumulating brain changes are, therefore, present prior to the clinical diagnosis of AD (i.e., in a “preclinical” stage) and should be evident if sensitive measures are used. A variety of neuro-protective agents designed to decelerate disease progression are either currently available or on the horizon (e.g., cholinesterase inhibitors, NMDA receptor antagonists, amyloid vaccine, non-steroidal anti-inflammatory drugs [NSAIDs], estrogen replacements, anti-oxidants), and, if such treatments are first employed when minimal neuropathology changes are present, they may retard or even forestall the disease process.
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