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@ARTICLE{Overall:140209,
author = {Overall, Rupert W and Kempermann, Gerd},
title = {{T}he {S}mall {W}orld of {A}dult {H}ippocampal
{N}eurogenesis.},
journal = {Frontiers in neuroscience},
volume = {12},
issn = {1662-453X},
address = {Lausanne},
publisher = {Frontiers Research Foundation},
reportid = {DZNE-2020-06531},
pages = {641},
year = {2018},
abstract = {Making mechanistic sense of genetically complex biological
systems such as adult hippocampal neurogenesis poses
conceptual and many practical challenges. Transcriptomics
studies have helped to move beyond single-gene approaches
and have greatly enhanced the accessibility to effects of
greater numbers of genes. Typically, however, the number of
experimental conditions compared is small and the
conclusions remain correspondingly limited. In contrast,
studying complex traits in genetic reference populations, in
which genetic influences are varied systematically, provides
insight into the architecture of relationships between
phenotypes and putative molecular mechanisms. We describe
that the correlation network among transcripts that builds
around the adult neurogenesis phenotype and its
endophenotypes is, as expected, a small-world network and
scale free. The high degree of connectivity implies that
adult neurogenesis is essentially an 'omnigenic' process.
From any gene of interest, a link to adult hippocampal
neurogenesis can be constructed in just a few steps. We show
that, at a minimum correlation of 0.6, the hippocampal
transcriptome network associated with adult neurogenesis
exhibits only two 'degrees of separation.' This fact has
many interesting consequences for our attempts to unravel
the (molecular) causality structure underlying adult
neurogenesis and other complex biological systems. Our
article is not written with the expert on network theory in
mind but rather aims to raise interest among
neurobiologists, active in neurogenesis and related fields,
in network theory and analysis as a set of tools that hold
great promise for coping with the study of 'omnigenic'
phenotypes and systems.},
cin = {AG Kempermann 1},
ddc = {610},
cid = {I:(DE-2719)1710001},
pnm = {342 - Disease Mechanisms and Model Systems (POF3-342)},
pid = {G:(DE-HGF)POF3-342},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:30294252},
pmc = {pmc:PMC6158315},
doi = {10.3389/fnins.2018.00641},
url = {https://pub.dzne.de/record/140209},
}