Table 1.
Authors | Omics considered | Biological sample | Clinical features of study cohort | Integrative method? | Findings |
---|---|---|---|---|---|
Beckmann et al. (2020) | Genomics | Brain tissue | AD | No | VGF is causally related to AD and is down regulated in patients. |
Transcriptomics | |||||
Chung et al. (2022) | Genomics | Brain tissue | AD | No | MGMT expression and methylation associated with AD pathology and risk. |
Transcriptomics | |||||
Clark et al. (2021) | Proteomics | Cerebrospinal fluid | AD and MCI | Yes | Distinct multi-omics molecular signatures differentially related to AD pathology. Biomarker candidates of AD and cognitive decline. |
Lipidomics | |||||
Metabolomics | |||||
Cohn et al. (2021) | Proteomics | Brain tissue | AD | No | In late AD tau and neuronal debris are resealed through extracellular vesicles. |
Transcriptomics | |||||
Lipidomics | |||||
Du et al. (2021) | Genomics | Plasma | AD and MCI | No | Genomic and transcriptomic biomarkers are associated with neuroimaging features |
Proteomics | |||||
Fang et al. (2022) | Genomics | Brain tissue | AD | No | Identification of 103 risk genes for AD. Three drugs associated with decreased risk of AD. |
Transcriptomics | |||||
Proteomics | |||||
Han et al. (2021) | Genomics | Brain tissue | AD | No | Web-based tool for visualisation of data |
Transcriptomics | |||||
Hu et al. (2020) | Genomics | Brain tissue | General population | Yes | Identification of 16 shared causal pathways between AD and Type 2 Diabetes |
Transcriptomics | |||||
Johnson et al. (2020) | Genomics | Brain tissue, Cerebrospinal fluid | General population | No | Microglial metabolism is associated with both normal ageing and AD and could serve a neuroprotective anti-inflammatory function. |
Proteomics | |||||
Johnson et al. (2022) | Genomics | Brain tissue | General population | No | APOEε4 and cognitive decline are not associated with the same biological pathways. |
Transcriptomics | |||||
Proteomics | |||||
Lefterov et al. (2019) | Transcriptomics | Brain tissue | AD | No | Differential association of APOE genotype with transcriptomic and lipidomic profiles in AD |
Lipidomics | |||||
Li et al. (2020) | Genomics | Brain tissue | AD and MCI | Yes | Prediction of PET-imaging outcomes improved by multi-omics modelling |
Transcriptomics | |||||
Li et al. (2021) | Genomics | Brain tissue | AD and MCI | Yes | Molecular subtypes are associated with MCI to AD conversion risk |
Transcriptomics | |||||
Madrid et al. (2021) | Genomics | Blood | AD | No | Glypican-2 (GPC2) protein downregulated in AD cases |
Transcriptomics | |||||
Min et al. (2021) | Genomics | Brain tissue | AD | No | Somatic mutations unlikely to be causal for AD |
Transcriptomics | |||||
Nativio et al. (2020) | Transcriptomics | Brain tissue | AD | No | AD affects the epigenome. Disease pathways are affected by chromatin and transcription regulation. |
Proteomics | |||||
Epigenomics | |||||
Odom et al. (2021) | Genomics | Brain tissue | AD | Yes | Most pathways involved in AD pathology are not picked up by single-omic approaches |
Transcriptomics | |||||
Park et al. (2022) | Genomics | Blood | AD and MCI | Yes | Identification of possible molecular drivers of AD heterogeneity or subtypes |
Transcriptomics | |||||
Proteomics | |||||
Peña-Bautista et al. (2021) | Genomics | Blood | AD and MCI | No | Lipids and miRNAs involved in fatty acids mechanisms associated with disease. |
Lipidomics | |||||
Rosenthal et al. (2022) | Genomics | Brain tissue | AD | No | Identification of 17 gene clusters of pathways altered in AD |
Transcriptomics | |||||
Ruffini et al. (2020) | Genomics | Brain tissue | AD | No | AD shares many proteomic and transcriptomic pathways with other neurodegenerative diseases |
Transcriptomics | |||||
Proteomics | |||||
Seyfried et al. (2017) | Genomics | Brain tissue | AD | No | Genetic risk loci for late-onset AD are preferentially enriched in microglia |
Transcriptomics | |||||
Proteomics | |||||
Shigemizu et al. (2020) | Genomics | Blood | MCI | No | Effective in MCI-to-AD conversion prediction model. |
Transcriptomics | |||||
Song et al. (2021) | Genomics | Blood | AD | No | 30 cross-omics blood-based biomarkers associated with AD. |
Transcriptomics | |||||
Proteomics | |||||
Tasaki et al. (2018) | Genomics | Brain tissue | General population | Yes | Specific set of neuronal genes to controls cognitive decline in older adults |
Transcriptomics | |||||
Tasaki et al. (2019) | Genomics | Brain tissue | General population | No | Cognitive and motor impairment could share an underlying genetic architecture |
Transcriptomics | |||||
Proteomics | |||||
Wang M. et al. (2021) | Genomics | Brain tissue | AD | Yes | Molecular signatures and gene networks identified for four brain regions. ATP6V1A is an important driver of AD. |
Transcriptomics | |||||
Wingo et al. (2022) | Genomics | Brain tissue | General population | No | Many of the neurodegenerative disease causal proteins are shared with psychiatric disorders |
Transcriptomics | |||||
Proteomics | |||||
Xicota et al. (2019) | Transcriptomics | Plasma | Memory clinic patients | Yes | Potential blood omics signature for prediction of amyloid positivity |
Metabolomics | |||||
Lipidomics | |||||
Xie et al. (2021) | Genomics | Brain tissue | General population | Yes | Discovery of multi-omic networks associated with brain function and neuroimaging. |
Transcriptomics | |||||
Proteomics | |||||
Xu et al. (2020) | Proteomics | Plasma | AD and MCI | No | Five lipid modules and 5 protein modules regulating homeostasis and innate immunity are strongly associated with AD. |
Lipidomics | |||||
Yu et al. (2022) | Transcriptomics | Blood, brain tissues | AD | No | Actin cytoskeleton is the most pronounced change in the cerebral cortex and serum of AD patients |
Proteomics | |||||
Zhou et al. (2021) | Genomics | Blood, brain tissues | AD | No | Useful tool for database browsing and network visualisation |
Transcriptomics | |||||
Proteomics |
AD, dementia of AD type; MCI, mild cognitive impairment.