ArticleHuman genetics2018
Genomic trade-offs: are autism and schizophrenia the steep price of the human brain?
Article in Human genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
26 citing papers in PubMed, 47 citations in OpenAlex.
- Tandem repeats in human brain evolution and disease susceptibility.Molecules and cells · 2026Review
- A General Principle of Neuronal Evolution Reveals a Human-Accelerated Neuron Type Potentially Underlying the High Prevalence of Autism in Humans.Molecular biology and evolution · 2025Article
- The cognitive science of language diversity: achievements and challenges.Cognitive processing · 2025Review
- Neurodevelopment Genes Encoding Olduvai Domains Link Myalgic Encephalomyelitis to Neuropsychiatric Disorders.Diagnostics (Basel, Switzerland) · 2025Article
- Molecular and micro-architectural mapping of gray matter alterations in psychosis.Molecular psychiatry · 2025Article
- A general principle of neuronal evolution reveals a human-accelerated neuron type potentially underlying the high prevalence of autism in humans.bioRxiv : the preprint server for biology · 2025Article
- Understanding the Emergence of Schizophrenia in the Light of Human Evolution: New Perspectives in Genetics.Genes, brain, and behavior · 2025Review
- Exploring the singularity of human neurons: keep calm and carry on.Frontiers in synaptic neuroscience · 2025Review
- Article
- Tandem NBPF 3mer HORs (Olduvai triplets) in Neanderthal and two novel HOR tandem arrays in human chromosome 1 T2T-CHM13 assembly.Scientific reports · 2023Article
- Proteolytic activation of human-specific Olduvai domains by the furin protease.International journal of biological macromolecules · 2023Article
- Genome-wide perturbations of Alu expression and Alu-associated post-transcriptional regulations distinguish oligodendroglioma from other gliomas.Communications biology · 2022Article
- Evolution and dysfunction of human cognitive and social traits: A transcriptional regulation perspective.Evolutionary human sciences · 2022Review
- Keeping the balance: Trade-offs between human brain evolution, autism, and schizophrenia.Frontiers in genetics · 2022Review
- Article
- Genomic selection signatures in autism spectrum disorder identifies cognitive genomic tradeoff and its relevance in paradoxical phenotypes of deficits versus potentialities.Scientific reports · 2021Article
- The influence of evolutionary history on human health and disease.Nature reviews. Genetics · 2021Review
- Genomic Variation, Evolvability, and the Paradox of Mental Illness.Frontiers in psychiatry · 2020Article
- The Driver of Extreme Human-Specific Olduvai Repeat Expansion Remains Highly Active in the Human Genome.Genetics · 2020Article
- Human core duplicon gene families: game changers or game players?Briefings in functional genomics · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Evolution often deals in genomic trade-offs: changes in the genome that are beneficial overall persist even though they also produce disease in a subset of individuals. Here, we explore the possibility that such trade-offs have occurred as part of the evolution of the human brain. Specifically, we provide support for the possibility that the same key genes that have been major contributors to the rapid evolutionary expansion of the human brain and its exceptional cognitive capacity also, in different combinations, are significant contributors to autism and schizophrenia. Furthermore, the model proposes that one of the primary genes behind this trade-off may not technically be "a gene" or "genes" but rather are the highly duplicated sequences that encode the Olduvai protein domain family (formerly called DUF1220). This is not an entirely new idea. Others have proposed that the same genes involved in schizophrenia were also critical to the rapid expansion of the human brain, a view that has been expressed as "the same 'genes' that drive us mad have made us human". What is new is that a "gene", or more precisely a protein domain family, has been found that may satisfy these requirements.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.