Dataset Information

Recent insights into viral infections as a trigger and accelerator in alzheimer's disease.

ABSTRACT: Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which only symptomatic medication is available, except for the recently FDA-approved aducanumab. This lack of effective treatment urges us to investigate alternative paths that might contribute to disease development. In light of the recent SARS-CoV-2 pandemic and the disturbing neurological complications seen in some patients, it is desirable to (re)investigate the viability of the viral infection theory claiming that a microbe could affect AD initiation and/or progression. Here, we review the most important evidence for this theory with a special focus on two viruses, namely HSV-1 and SARS-CoV-2. Moreover, we discuss the possible involvement of extracellular vesicles (EVs). This overview will contribute to a more rational approach of potential treatment strategies for AD patients.

SUBMITTER: De Vlieger L

PROVIDER: S-EPMC9385395 | biostudies-literature | 2022 Aug

REPOSITORIES: biostudies-literature

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Recent insights into viral infections as a trigger and accelerator in alzheimer's disease.

De Vlieger Lize L Vandenbroucke Roosmarijn E RE Van Hoecke Lien L

Drug discovery today 20220818 11

Alzheimer's disease (AD) is a progressive neurodegenerative disorder for which only symptomatic medication is available, except for the recently FDA-approved aducanumab. This lack of effective treatment urges us to investigate alternative paths that might contribute to disease development. In light of the recent SARS-CoV-2 pandemic and the disturbing neurological complications seen in some patients, it is desirable to (re)investigate the viability of the viral infection theory claiming that a mi ...[more]

PMID: 35987492

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Project description:IntroductionRecent advances in generating massive single-cell/nucleus transcriptomic data have shown great potential for facilitating the identification of cell type-specific Alzheimer's disease (AD) pathobiology and drug-target discovery for therapeutic development.MethodsWe developed The Alzheimer's Cell Atlas (TACA) by compiling an AD brain cell atlas consisting of over 1.1 million cells/nuclei across 26 data sets, covering major brain regions (hippocampus, cerebellum, prefrontal cortex, and so on) and cell types (astrocyte, microglia, neuron, oligodendrocytes, and so on). We conducted nearly 1400 differential expression comparisons to identify cell type-specific molecular alterations (e.g., case vs healthy control, sex-specific, apolipoprotein E (APOE) ε4/ε4, and TREM2 mutations). Each comparison was followed by protein-protein interaction module detection, functional enrichment analysis, and omics-informed target and drug (over 700,000 perturbation profiles) screening. Over 400 cell-cell interaction analyses using 6000 ligand-receptor interactions were conducted to identify the cell-cell communication networks in AD.ResultsAll results are integrated into TACA (https://taca.lerner.ccf.org/), a new web portal with cell type-specific, abundant transcriptomic information, and 12 interactive visualization tools for AD.DiscussionWe envision that TACA will be a highly valuable resource for both basic and translational research in AD, as it provides abundant information for AD pathobiology and actionable systems biology tools for drug discovery.HighlightsWe compiled an Alzheimer's disease (AD) brain cell atlas consisting of more than 1.1 million cells/nuclei transcriptomes from 26 data sets, covering major brain regions (cortex, hippocampus, cerebellum) and cell types (e.g., neuron, oligodendrocyte, astrocyte, and microglia).We conducted over 1400 differential expression (DE) comparisons to identify cell type-specific gene expression alterations. Major comparison types are (1) AD versus healthy control; (2) sex-specific DE, (3) genotype-driven DE (i.e., apolipoprotein E [APOE] ε4/ε4 vs APOE ε3/ε3; TREM2R47H vs common variants) analysis; and (4) others. Each comparison was further followed by (1) human protein-protein interactome network module analysis, (2) pathway enrichment analysis, and (3) gene-set enrichment analysis.For drug screening, we conducted gene set enrichment analysis for all the comparisons with over 700,000 drug perturbation profiles connecting more than 10,000 human genes and 13,000 drugs/compounds.A total of over 400 analyses of cell-cell interactions against 6000 experimentally validated ligand-receptor interactions were conducted to reveal the disease-relevant cell-cell communications in AD.

Dataset Information

Recent insights into viral infections as a trigger and accelerator in alzheimer's disease.

Publications

Recent insights into viral infections as a trigger and accelerator in alzheimer's disease.

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