Synaptic Pathology of Down Syndrome
Abstract
Down syndrome is characterized by mild to moderate cognitive impairments that are caused by trisomy of chromosome 21. Several anatomical, behavioral, electrophysiological, and developmental abnormalities have been associated with Down syndrome. In this review, the current knowledge about the neurobiology of this disease and future perspectives of pharmacological treatments for this condition will be discussed.
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Deficient synaptogenesis and synaptic function are thought to be key drivers of intellectual disability in Down syndrome.
“Deficient synaptogenesis and synaptic function are thought to be key drivers of intellectual disability in DS111 (Fig. 3).”
From Consequences of trisomy 21 for brain development in Down syndrome (2024) · cites this paper as [111]
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References 133 · Cited by 33
- Authors
- Garner, C. C., & Wetmore, D. Z.
- Affiliations
- Stanford Medicine (US)
- Corresponding author
- Garner, Craig C.
- ORCID
- Garner, Craig C.
- Venue
- Advances in Experimental Medicine and Biology
- Publisher
- Springer Vienna
- Published
- 2012
- Volume
- 970
- Pages
- 451-468
- ISSN
- 0065-2598 (ISSN-L)
- OpenAlex
- W99742205
- Cited by
- 33
- References
- 133
- Citations by year
- 2026: 2 · 2024: 1 · 2023: 3 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 1 · 2017: 2 · 2016: 5 · 2015: 1 · 2014: 6 · 2013: 5 · 2012: 1
- FWCI
- 10.39
- Type
- book chapter
- Language
- en
- Open access
- closed
- Licence
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Keywords
- Down syndrome, synaptic pathology, cognitive impairment, neurobiology, pharmacotherapy, synaptic dysfunction
- MeSH terms
- Animals, Chromosomes, Human, Pair 21, Disease Models, Animal, Down Syndrome, Gene Expression Regulation, Hippocampus, Humans, Mice, Transgenic, Synaptic Transmission, Synapses, Trisomy, Receptors, N-Methyl-D-Aspartate, N-Methylaspartate, Long-Term Potentiation, Mice, Molecular Targeted Therapy
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