Mild cognitive impairment - an early stage of Alzheimer's disease?

Citation
O. Almkvist et al., Mild cognitive impairment - an early stage of Alzheimer's disease?, J NEURAL TR, 1998, pp. 21-29
Citations number
47
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEURAL TRANSMISSION
ISSN journal
03009564 → ACNP
Year of publication
1998
Supplement
54
Pages
21 - 29
Database
ISI
SICI code
0300-9564(1998):<21:MCI-AE>2.0.ZU;2-T
Abstract
The hypothesis that mild cognitive impairment (MCI) represents an early sta ge of Alzheimer's disease (AD) was investigated by reviewing recent researc h from three sources: asymptomatic and symptomatic individuals carrying mut ations that cause AD, hospital-samples of non-demented patients with MCI at the initial examination that are followed longitudinally, and community-ba sed incident cases of AD. Studies with asymptomatic mutation carriers of the amyloid precursor protei n and presenilin 1 gene have shown a linear and disease-related decline in most cognitive functions that begins approximately 10 years before the expe cted clinical onset of AD. However, there is considerable overlap between t he level of impairment for mutation carriers and non-carriers of the same a ge during the early preclinical stage of AD. Hospital-based longitudinal st udies have shown that non-demented individuals with isolated mild episodic memory impairment may develop clinically diagnosed AD with widespread cogni tive deficits in a few years time. Community-based epidemiological studies on the incidence of AD demonstrate that indices of episodic memory, in addi tion to measures of general cognitive functioning, are useful in predicting early AD. In contrast, subjective memory impairment or age-associated memo ry impairment are less powerful predictors of future dementia development. In summary, there is converging evidence to demonstrate that preclinical AD is characterized by a common behavioral phenotype, with cognitive decline in several domains, predominantly in episodic memory. The decline appears t o start many years before the clinical onset of AD. Moreover, the progressi on of the impairment appears to be continuous. Finally, this pattern of per formance generalizes across etiology of AD (familial or sporadic), clinical onset (early or late), sample composition (hospital or community), and met hod of assessment.