Dendritic structural plasticity and neuropsychiatric disease
Open accessAbstract
The structure of neuronal circuits that subserve cognitive functions in the brain is shaped and refined throughout development and into adulthood. Evidence from human and animal studies suggests that the cellular and synaptic substrates of these circuits are atypical in neuropsychiatric disorders, indicating that altered structural plasticity may be an important part of the disease biology. Advances in genetics have redefined our understanding of neuropsychiatric disorders and have revealed a spectrum of risk factors that impact pathways known to influence structural plasticity. In this Review, we discuss the importance of recent genetic findings on the different mechanisms of structural plasticity and propose that these converge on shared pathways that can be targeted with novel therapeutics.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
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?
Some neurodevelopmental diseases that impair higher cognitive functions, such as intellectual disability and autism spectrum disorder, may involve accelerated brain development.
“Conversely, some neurodevelopmental diseases (NDDs) that impair higher cognitive functions, such as intellectual disability (ID) and autism spectrum disorder (ASD), may involve accelerated brain development.10,11,12,13”
From Synaptic neoteny of human cortical neurons requires species-specific balancing of SRGAP2-SYNGAP1 cross-inhibition (2024) · cites this paper as [11]
The ‘Spine pathology in autism spectrum disorder’ section reports brain and cortical grey-matter enlargement beginning before age two, alongside an overabundance of spines, which is consistent with atypically increased early growth in ASD. The ‘Spine pathology in intellectual disability’ section instead describes immature spines and reduced dendritic complexity; it does not support accelerated brain development in intellectual disability. Neither section establishes an accelerated rate of overall brain development. (LLM, conf=0.84)
Experimental — accuracy not yet measuredPrecocious brain development was previously associated with specific forms of NDD, including ASD.
“Precocious brain development was previously associated with specific forms of NDD, including ASD,11,61 and in vitro PSC models have recently suggested altered timing of neuronal differentiation in some forms of ASD.62”
From Synaptic neoteny of human cortical neurons requires species-specific balancing of SRGAP2-SYNGAP1 cross-inhibition (2024) · cites this paper as [11]
Synaptic dysfunction and altered synaptic plasticity are closely associated with neurologic and psychiatric disorders.
“Synaptic dysfunction and altered synaptic plasticity are closely associated with neurologic and psychiatric disorders (Goto et al., 2010;Forrest et al., 2018;Wang et al., 2018).”
From Psychedelics and Neural Plasticity: Therapeutic Implications (2022) · cites this paper as Forrest et al., 2018
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 303 · Cited by 464
- Authors
- Forrest, M. P., Parnell, E., & Penzes, P.
- Affiliations
- Northwestern University (US)
- Corresponding author
- Penzes, Peter
- Venue
- Nature Reviews Neuroscience
- Published
- 2018-03-16
- Volume
- 19
- Issue
- 4
- Pages
- 215-234
- ISSN
- 1471-003X (ISSN-L)
- 1471-0048
- PMC
- PMC6442683
- OpenAlex
- W2792523657
- Cited by
- 464
- References
- 303
- Citations by year
- 2026: 28 · 2025: 45 · 2024: 66 · 2023: 49 · 2022: 68 · 2021: 87 · 2020: 63 · 2019: 42 · 2018: 14 · 2016: 1
- FWCI
- 6.86
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Mental Health (R01MH097216, R01MH071316, R01MH107182)
- National Institute of Neurological Disorders and Stroke (R01NS100785)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Neurodevelopmental Disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- dendritic spines, dendritic morphology, neuropsychiatric disorders, activity-dependent plasticity, neural circuit development, genetic risk factors, therapeutic target
- MeSH terms
- Animals, Mental Disorders, Brain, Dendrites, Humans, Nerve Tissue Proteins, Neuronal Plasticity, Risk Factors, Genetic Predisposition to Disease
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
