Cited by 290Down syndrome and intellectual disability researchAlzheimer's disease research and treatmentsDementia and Cognitive Impairment Research

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Aging in Down Syndrome and the Development of Alzheimer's Disease Neuropathology

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Head, Elizabeth, T. Lott, Ira, M. Wilcock, Donna, A. Lemere, Cynthia·2015·Current Alzheimer Research

DOI 10.2174/1567205012666151020114607PMC PMC4948181

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Abstract

Chromosome 21, triplicated in Down Syndrome, contains several genes that are thought to play a critical role in the development of AD neuropathology. The overexpression of the gene for the amyloid precursor protein (APP), on chromosome 21, leads to early onset beta-amyloid (Aβ) plaques in DS. In addition to Aβ accumulation, middle-aged people with DS develop neurofibrillary tangles, cerebrovascular pathology, white matter pathology, oxidative damage, neuroinflammation and neuron loss. There is also evidence of potential compensatory responses in DS that benefit the brain and delay the onset of dementia after there is sufficient neuropathology for a diagnosis of AD. This review describes some of the existing literature and also highlights gaps in our knowledge regarding AD neuropathology in DS. It will be critical in the future to develop networked brain banks with standardized collection procedures to fully characterize the regional and temporal pathological events associated with aging in DS. As more information is acquired regarding AD evolution in DS, there will be opportunities to develop interventions that are age-appropriate to delay AD in DS.

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Authors: Head, E., T. Lott, I., M. Wilcock, D., & A. Lemere, C.
Affiliations: University of Kentucky (US)
ORCID: Head, Elizabeth
Venue: Current Alzheimer Research
Publisher: Bentham Science Publishers Ltd.
Published: 2015-12-07
Volume: 13
Issue: 1
Pages: 18-29
ISSN: 1567-2050 (ISSN-L)
DOI: 10.2174/1567205012666151020114607
PMC: PMC4948181
OpenAlex: W2190781699
Cited by: 289
References: 160
Citations by year: 2026: 13 · 2025: 30 · 2024: 23 · 2023: 14 · 2022: 18 · 2021: 34 · 2020: 29 · 2019: 29 · 2018: 55 · 2017: 32 · 2016: 10 · 2015: 1
FWCI: 35.03
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Current Alzheimer Research (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
eScholarship (California Digital Library) (submittedVersion, cc-by)
Funders: National Institutes of Health
National Institute on Aging (R01AG040092, P50AG016573, R01AG16573)
National Institute of Neurological Disorders and Stroke (NS079637, R01NS079637, R01NS136122)
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD065160, R01HD064993)
Topics: Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Down syndrome, Alzheimer's disease, Alzheimer's disease pathology, aging, chromosome 21, amyloid precursor protein, amyloid plaques, neurofibrillary tangles, cerebrovascular pathology, white matter pathology, oxidative damage, neuroinflammation, neuronal loss, dementia onset, brain banks
MeSH terms: Neuropathology, Age Factors, Aging, Alzheimer Disease, Animals, Down Syndrome, Humans, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, tau Proteins

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Aging in Down Syndrome and the Development of Alzheimer's Disease Neuropathology

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