Correction: 'She lifted me up': kinship construction in human-AI resilient communication among Chinese users.

Brain-related disorders and diseases are common and have high lifetime prevalences. For instance, one in eight people in the world live with a psychiatric disorder (), and the lifetime risk of receiving a diagnosis of Alzheimer's disease (AD) or Parkinson's disease (PD) is up to one in five (; ; ). Furthermore, psychiatric and neurodegenerative conditions are often co-occurring (; ; ; ). These brain-related conditions, including neurodevelopmental disorders, psychiatric disorders, and neurodegenerative diseases, are multifactorial, involving both genetic as well as environmental factors in their development and persistence (; ; ; ; ). Considerable knowledge about the molecular underpinnings of many brain-related diseases is lacking, and effective treatments for most of these conditions are not available yet. Previous studies on postmortem brain samples have identified potential roles of specific brain cell types in different brain-related conditions, likely related to their specific functions. Neurons are the main brain cells that receive and send information; glial cells have a supporting role in the central nervous system: microglia and astrocytes are important effector cells in the central immune system (), whereas the main role of oligodendrocytes is to myelinate neurons (). The combination of differences in both the proportions of brain cell types and their actual cellular function in brain-related diseases is found for a number of cell types. For example, alterations in microglia proportions and microglial gene expression levels have been observed for autism spectrum disorder, schizophrenia, depression, and AD (; ; ; ; ). Similar differences in gene expression levels have been observed for astrocytes in depression (), and for gene expression levels in neuronal cells in autism spectrum disorder, schizophrenia, and PD, as well as cellular functionality and morphological differences in depression (; ; ; ). From a related, yet conceptually different perspective based on genome-, transcriptome-, and epigenome-wide association studies, genetic and epigenetic loci associated with brain-related conditions are enriched in different brain cell types: schizophrenia has been shown to be associated with median spiny neurons () and GABA- and glutamatergic neurons (). Similar enrichment studies for ADHD have shown associations with excitatory neurons and astrocytes (; ), while PD has been associated with oligodendrocytes through genetic enrichment in cell-specific expression datasets (). Collectively, this emerging evidence provides compelling examples that different brain-related conditions are linked to changes in a distinct palette of brain cell type proportions and functions. This then raises the opportunity that studying brain cell type composition more broadly might contribute an important layer to a better understanding of brain disease etiology. Cell type identity, function, and regulation are modulated, in part, by modifications of the chromatin landscape, often referred to as epigenetics. Of these, at least in human populations, DNA methylation (DNAm) is best understood. DNAm patterns are tissue- and cell type-specific (), and tend to be more stable than transcriptomics signatures (; ; ). However, most DNAm-association studies on brain-related outcomes are performed in surrogate tissues such as blood. In living humans, the single most important reason for the choice of peripheral samples over brain samples is practicality related to less invasive collection protocols (). That said, given the major relation of DNAm patterns with tissue and cellular identify, it is clear that peripheral blood samples might not fully report on brain DNAm. This has been substantiated by previous studies documenting that the relationship between DNAm in peripheral surrogate tissue and brain issue is rather complex. On the one hand, DNAm levels show statistically significant global correlations between peripheral blood and brain tissue across all measured DNAm sites (Pearson's r = 0.860 and r = 0.892), although this might be skewed by the inclusion of non-variable DNAm sites (; ; ; ). On the other hand, at the level of individual peripheral DNAm sites, only 6-11% showed moderate to high blood-brain DNAm level correlations (; ; ; ). Despite the cell type- and tissue-specificity of DNAm, the correlation of DNAm sites across tissues suggests that some peripheral blood DNAm sites can still be informative for brain DNAm levels, as documented to various degrees in previous studies. On that basis, single DNAm sites with high blood-brain correlation might lead towards informative biomarkers for brain-related phenotypes. Supporting this notion, epigenome-wide association studies have identified DNAm sites that are significantly associated with different brain disorders using peripheral samples (; ; ; ; ; ; ).