Postnatal Cytoarchitecture and neurochemical hippocampal dysfunction in Down Syndrome
Open accessAbstract
Although the prenatal hippocampus displays deficits in cellular proliferation/migration and volume, which are later associated with memory deficits, little is known about the effects of trisomy 21 on postnatal hippocampal cellular development in Down syndrome (DS). We examined postnatal hippocampal neuronal profiles from autopsies of DS and neurotypical (NTD) neonates born at 38-weeks’-gestation up to children 3 years of age using antibodies against non-phosphorylated (SMI-32) and phosphorylated (SMI-34) neurofilament, calbindin D-28k (Calb), calretinin (Calr), parvalbumin (Parv), doublecortin (DCX) and Ki-67, as well as amyloid precursor protein (APP), amyloid beta (Aβ) and phosphorylated tau (p-tau). Although the distribution of SMI-32-immunoreactive (-ir) hippocampal neurons was similar at all ages in both groups, pyramidal cell apical and basal dendrites were intensely stained in NTD cases. A greater reduction in the number of DCX-ir cells was observed in the hippocampal granule cell layer in DS. Although the distribution of Calb-ir neurons was similar between the youngest and oldest NTD and DS cases, Parv-ir was not detected. Conversely, Calr-ir cells and fibers were observed at all ages in DS, while NTD cases displayed mainly Calr-ir fibers. Hippocampal APP/Aβ-ir diffuse-like plaques were seen in DS and NTD. By contrast, no Aβ1–42 or p-tau profiles were observed. These findings suggest that deficits in hippocampal neurogenesis and pyramidal cell maturation and increased Calr immunoreactivity during early postnatal life contribute to cognitive impairment in DS.
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Reduced neurogenesis occurs in both humans with DS-AD and DS mouse models.
“We expected to find specific alterations in the DG due to reduced neurogenesis in both humans with DS‐AD and DS mouse models. 38 , 39”
From Disruption of hippocampal upstream regulators of mTOR and insulin pathways in Down syndrome with Alzheimer's disease neuropathology: Preliminary observations (2026) · cites this paper as [39]
The Introduction reports impaired neurogenesis in human DS fetuses and restoration of neurogenesis after treatment in a Ts65Dn DS mouse model. The Discussion (§4.1) also suggests a postnatal neurogenesis/migration deficit in children with DS. These passages concern developmental DS, not humans with DS-associated Alzheimer’s disease (DS-AD), so the human population specified in the claim is not supported. (LLM, conf=0.87)
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- Authors
- Moreno, D. G., Utagawa, E. C., Arva, N. C., Schafernak, K. T., Mufson, E. J., & Perez, S. E.
- Affiliations
- Barrow Neurological Institute (US)
- Lurie Children's Hospital (US)
- Phoenix Children's Hospital (US)
- Corresponding author
- Perez, Sylvia E.
- Venue
- Journal of Clinical Medicine
- Publisher
- MDPI AG
- Published
- 2021-07-31
- Volume
- 10
- Issue
- 15
- Pages
- 3414
- ISSN
- 2077-0383 (ISSN-L)
- PMC
- PMC8347520
- OpenAlex
- W3189811284
- Cited by
- 7
- References
- 78
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 2 · 2022: 2 · 2021: 1
- FWCI
- 1.08
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Journal of Clinical Medicine (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute on Aging (P01AG014449, R01AG061566)
- BrightFocus Foundation (CA2018010)
- Arizona Alzheimer’s Consortium (P30AG010161)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- Down syndrome, hippocampus, postnatal development, hippocampal neurogenesis, doublecortin, calretinin, parvalbumin, calbindin-D28k, amyloid plaques, amyloid-beta, phosphorylated tau, neuronal cytoarchitecture, cognitive impairment, neonates
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Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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