Cited by 214Alzheimer's disease research and treatmentsDown syndrome and intellectual disability researchDementia and Cognitive Impairment Research

Early Amyloid Deposition in the Medial Temporal Lobe of Young Down Syndrome Patients: A Regional Quantitative Analysis

Leverenz, James B., Raskind, Murray A.·1998·Experimental Neurology

Abstract

The presence of the neuropathological alterations of Alzheimer's disease (AD) in essentially all older Down syndrome (DS) patients suggests that the examination of younger DS patients may clarify the early pathological progression of AD. We examined the hippocampus and parahippocampal-inferior temporal gyri of 42 DS patients (ages 4 days to 38 years) for the deposition of amyloid beta protein (Abeta) using both a modified Bielschowsky stain and immunohistochemistry for Abeta protein. The parahippocampal and inferior temporal gyri demonstrated Abeta staining in cases as young as 8 years of age. As age and degree of Abeta deposition increased, staining included the CA-1/subiculum and dentate molecular layer followed then by the remainder of the CA hippocampal regions. The first neuritic plaques were observed in the CA-1/subiculum, despite this being a later region of Abeta deposition. Although Abeta staining increased with age, there was substantial variability in the severity of Abeta deposition within age groups. These results suggest that within the hippocampal/parahippocampal region there is a progressive stereotypic deposition of Abeta. The variable severity of Abeta deposition within age groups suggests that other factors, besides DS, may be contributing to the timing and severity of Abeta deposition.

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Crossref · 10.1006/exnr.1997.6777

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  • Individuals with Down syndrome (T21) are strongly predisposed to Alzheimer's disease, with nearly all exhibiting AD-related neuropathological features by age ∼40 and highly variable onset of dementia thereafter.

    “Individuals with Down syndrome (DS), caused by trisomy of chromosome 21 (chr21, T21), are strongly predisposed to Alzheimer’s disease (AD), due to triplication of the APP gene, with ∼100% penetrance of AD brain pathology by age 40 and variable onset of dementia thereafter.”

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Authors
Leverenz, J. B., & Raskind, M. A.
Affiliations
University of Washington (US)
Venue
Experimental Neurology
Publisher
Elsevier BV
Published
1998-04
Volume
150
Issue
2
Pages
296-304
ISSN
0014-4886 (ISSN-L)
OpenAlex
W1994573232
Cited by
214
References
33
Citations by year
2026: 3 · 2025: 9 · 2024: 10 · 2023: 10 · 2022: 9 · 2021: 14 · 2020: 9 · 2019: 11 · 2018: 7 · 2017: 12 · 2016: 4 · 2015: 15 · 2014: 17 · 2013: 7 · 2012: 9
FWCI
3.07
Type
journal article
Language
en
Open access
closed
Locations
  • Experimental Neurology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • AGE-WELL
  • Ministerul Cercetării, Inovării şi Digitalizării
  • National Institute on Aging (AG 05136, AG00503, P50AG005136)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
Down syndrome, amyloid-beta deposition, Alzheimer's disease, medial temporal lobe, hippocampus, parahippocampal gyrus, inferior temporal gyrus, neuritic plaques
MeSH terms
Adolescent, Adult, Age Factors, Aged, Aging, Alzheimer Disease, Child, Child, Preschool, Down Syndrome, Female, Hippocampus, Humans, Immunohistochemistry, Infant, Infant, Newborn, Male, Organ Specificity, Reference Values, Regression Analysis, Temporal Lobe, Amyloid beta-Peptides

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