Dendritic and histochemical development and ageing in patients with Down's syndrome
Abstract
ABSTRACT. Mental retardation and dementia characteristic of Down's syndrome (DS) have a complex pathogenesis. Golgi and immunohistochemical studies were done on DS patients and controls from foetuses and elderly adults. Golgi studies on the cerebral cortex revealed that the postsynaptic spines on the basal dendrites increase from neonate to 15 years of age and gradually decrease after 20 years in controls, but poorly increase in children and rapidly decrease in adults with DS. This deficient synaptogenesis and dendritic atrophy may be related to mental retardation. On the other hand, immunohistochem‐istry on proteins, whose genes are located on chromosome 21, revealed that c‐temiinal protein of beta‐amyloid appears in neurons of DS, S‐100‐positive glia increases in the hippocampus of neonates and adults, and membrane protein OK‐2 is expressed earlier and is more widespread in the DS brains. The overexpression and early appearance of gene products in DS brains may be related to the pathogenesis of or predisposition to mental disorders or to dendritic hypogenesis.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The spines that are present in Down syndrome exhibit morphological anomalies, such as abnormally small and exceptionally long, thin spines.
“Moreover, the spines that are present exhibit morphological anomalies, such as abnormally small and exceptionally long, thin spines115–118 (Fig. 3a).”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [118]
The earliest reports using Golgi staining of human brain tissue provided consistent evidence that newborns and infants with Down syndrome have substantial deficits in spine density and abnormal spine morphology.
“The earliest reports using Golgi staining of human brain tissue provided consistent evidence that newborns and infants with DS have substantial deficits in spine density and abnormal spine morphology115–118.”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [118]
These differences are present across the cortical laminae.
“These differences are present across the cortical laminae115–118.”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [118]
Neurons from both the motor and visual cortices of infants with Down syndrome as young as 2 months of age have fewer dendritic spines.
“Specifically, neurons from both the motor and visual cortices of infants with DS as young as 2 months of age have fewer dendritic spines117,118.”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [118]
Cites
Amyloid β Protein Gene: cDNA, mRNA Distribution, and Genetic Linkage Near the Alzheimer Locus
Tanzi, R. E., Gusella, J. F., Watkins, P. C., Bruns, G. A. P., St George-Hyslop, P., Van Keuren, M. L., Patterson, D., Pagan, S., Kurnit, D. M., & Neve, R. L. (1987) · Science · doi:10.1126/science.2949367 · Cited by 1,611 · see citing works
Dendritic atrophy in children with down’s syndrome.
Becker, L. E., Armstrong, D. L., & Chan, F. (1986) · Annals of Neurology · doi:10.1002/ana.410200413 · Cited by 279 · see citing works
Down's syndrome: Is there a decreased population of neurons?
Ross, M. H., Galaburda, A. M., & Kemper, T. L. (1984) · Neurology · doi:10.1212/wnl.34.7.909 · Cited by 191 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Dendritic Spine Pathology: Cause or Consequence of Neurological Disorders?
Fiala, J. C., Spacek, J., & Harris, K. M. (2002) · Brain Research Reviews · doi:10.1016/s0165-0173(02)00158-3 · Cited by 811 · see citing works
Dendritic Spine Structural Anomalies in Fragile-X Mental Retardation Syndrome
Irwin, S. A. (2000) · Cerebral Cortex · doi:10.1093/cercor/10.10.1038 · Cited by 626 · see citing works
Serotonin and brain development: role in human developmental diseases
Whitaker-Azmitia, P. M. (2001) · Brain Research Bulletin · doi:10.1016/s0361-9230(01)00615-3 · Cited by 506 · see citing works
Bhatt, D. H., Zhang, S., & Gan, W.-B. (2009) · Annual Review of Physiology · doi:10.1146/annurev.physiol.010908.163140 · Cited by 380 · see citing works
What happens to your brain on the way to Mars
Parihar, V. K., Allen, B., Tran, K. K., Macaraeg, T. G., Chu, E. M., Kwok, S. F., Chmielewski, N. N., Craver, B. M., Baulch, J. E., Acharya, M. M., et al. (2015) · Science Advances · doi:10.1126/sciadv.1400256 · Cited by 217 · see citing works
Trisomy-driven overexpression of DYRK1A kinase in the brain of subjects with down syndrome
Dowjat, W. K., Adayev, T., Kuchna, I., Nowicki, K., Palminiello, S., Hwang, Y. W., & Wegiel, J. (2007) · Neuroscience Letters · doi:10.1016/j.neulet.2006.11.026 · Cited by 190 · see citing works
Communication breaks-Down: From neurodevelopment defects to cognitive disabilities in Down syndrome
Contestabile, A., Benfenati, F., & Gasparini, L. (2010) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2010.01.003 · Cited by 134 · see citing works
Garcia, O., Torres, M., Helguera, P., Coskun, P., & Busciglio, J. (2010) · PLoS ONE · doi:10.1371/journal.pone.0014200 · Cited by 122 · see citing works
Genome-wide expression studies in Autism spectrum disorder, Rett syndrome, and Down syndrome
Lintas, C., Sacco, R., & Persico, A. M. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2010.11.010 · Cited by 96 · see citing works
Dendritic and Synaptic Protection: Is It Enough to Save the Retinal Ganglion Cell Body and Axon?
Morquette, J. B., & Di Polo, A. (2008) · Journal of Neuro-Ophthalmology · doi:10.1097/wno.0b013e318177edf0 · Cited by 51 · see citing works
Ponroy Bally, B., Farmer, W. T., Jones, E. V., Jessa, S., Kacerovsky, J. B., Mayran, A., Peng, H., Lefebvre, J. L., Drouin, J., Hayer, A., et al. (2020) · Human Molecular Genetics · doi:10.1093/hmg/ddaa003 · Cited by 49 · see citing works
Consequences of trisomy 21 for brain development in Down syndrome
Russo, M. L., Sousa, A. M. M., & Bhattacharyya, A. (2024) · Nature Reviews Neuroscience · doi:10.1038/s41583-024-00866-2 · Cited by 28 · see citing works
“These differences are present across the cortical laminae 115–118 .”
Influential
- Authors
- TAKASHIMA, S., IIDA, K., MITO, T., & ARIMA, M.
- Affiliations
- National Center of Neurology and Psychiatry (JP)
- Corresponding author
- TAKASHIMA, S.
- Venue
- Journal of Intellectual Disability Research
- Publisher
- Wiley
- Published
- 1994-06
- Volume
- 38
- Issue
- 3
- Pages
- 265-273
- ISSN
- 0964-2633 (ISSN-L)
- 1365-2788
- OpenAlex
- W2010103259
- Cited by
- 126
- References
- 3
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 6 · 2023: 2 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 4 · 2018: 5 · 2017: 5 · 2015: 6 · 2014: 6 · 2013: 6 · 2012: 5
- FWCI
- 3.55
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Intellectual Disability Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- Down syndrome, dendritic development, dendritic atrophy, postsynaptic spines, synaptogenesis, intellectual disability, dementia, aging, chromosome 21 genes, amyloid-beta, S-100 protein, hippocampus, cerebral cortex
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Alzheimer Disease, Cell Count, Cerebral Cortex, Child, Child, Preschool, Dendrites, Down Syndrome, Female, Gestational Age, Hippocampus, Humans, Immunoenzyme Techniques, Infant, Infant, Newborn, Male, Membrane Proteins, Middle Aged, S100 Proteins, Neurons, Pregnancy, Synapses, Amyloid beta-Peptides, Neurofibrillary Tangles, Cellular Senescence
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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 ›
Are you an author, or do you see a problem with this page? Request a review
