ISSN:
1432-0533
Keywords:
Key words Down’s syndrome
;
Alzheimer’s disease
;
Entorhinal cortex
;
Neurofibrillary pathology
;
Neuronal loss
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract In Alzheimer’s disease (AD), neurofibrillary degeneration of neurons starts in the transentorhinal cortex and spreads in a time-dependent manner to the entorhinal cortex, which provides a major input to the hippocampus – a key structure of the memory system. People with Down’s syndrome (DS) develop neurofibrillary changes more than 30 years earlier than those with sporadic AD. To characterize AD-related pathology in the entorhinal cortex in DS, we examined seven subjects with DS of 60–74 years of age who died in the end stage of AD, and four age-matched control subjects. The volume of the entorhinal cortex in brains of subjects with DS was 42% less than that in control cases; however, the total number of neurons free of neurofibrillary changes was reduced in DS by 90%: from 9,619,000 ± 914,000 (mean ± standard deviation) to 932,000 ± 504,000. The presence of 2,488,000 ± 544,000 neurofibrillary tangles in the entorhinal cortex of people with DS, the prevalence of end-stage tangles, and the significant negative correlation between the total number of intact neurons and the percentage of neurons with neurofibrillary changes indicate that neurofibrillary degeneration is a major cause of neuronal loss in the entorhinal cortex of people with DS. The relatively low amyloid load (7 ± 1%) and lack of correlation between the amyloid load and the volumetric or neuronal loss suggest that the contribution of β-amyloid to neuronal loss in the entorhinal cortex is unsubstantial.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004010050968
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