The terrible week for creationism continues unabated: Following yesterday’s news of more evidence of common descent of the great apes, including humans, we have news that creationism's putative designer has apparently given some people a gene variant that increases their risk of developing Alzheimer’s dementia in later life, while some others get a variant the reduces that risk.
A problem of creationists' own making is the insistence that mutations don't happen by chance but need the deliberate intervention of their favourite putative designer, without whom nothing happens.
This means they need to ignore the existence of parasites, which, if they were designed deliberately, can only be regarded as evidence that whatever designed them had malevolent intent, and intended to increase the suffering in the world, since that is what they do.
It also means they need to ignore the evidence that a lot of diseases are caused by mutations, especially the degenerative diseases in older people, which don't manifest until after they have produced their offspring, and so passed on their genetics, including any mutations.
This is where we come to the news that a large team of researchers, led by scientists from Indiana University School of Medicine, USA, have identified a mutation in a critical gene for the brain's immune system, so greatly increasing the risk of developing Alzheimer's.
The immune system is just one of the integrated bodily systems that creationists often cite as evidence of intelligent design, because, in their simplistic and parochial view of the world, if they can’t understand how something happened, it must have been done by the locally-popular god their parents believed in. This requires them to ignore the many problems that the immune system causes because of its propensity to turn on the body it is supposedly designed to protect, and the many examples of how it fails in its function because parasites have been 'designed' to get past it.
The investigating team found two variants of the PLCG2 (phospholipase C-Gamma-2) genes: the M28L variant which increases the risk of Alzheimer's; and the P522R variant which reduces the risk. Any intelligent, benevolent designer who wanted to reduce the risk would have given us the P522R variant. Instead, if we believe creationists, it chose to give that to some, but others got the M28L variant.
The team’s research is published open access in the journal Immunity:
Highlights
- M28L variant of PLCG2 is associated with an increased risk for Alzheimer’s disease (AD)
- In an amyloidogenic AD mouse model, PLCG2M28L exacerbates disease pathogenesis
- Conversely, PLCG2P522R, a protective PLCG2 variant, attenuates AD pathogenesis
- The PLCG2 variants uniquely alter the microglial transcriptome and phenotypes
Summary
Genetic association studies have demonstrated the critical involvement of the microglial immune response in Alzheimer’s disease (AD) pathogenesis. Phospholipase C-gamma-2 (PLCG2) is selectively expressed by microglia and functions in many immune receptor signaling pathways. In AD, PLCG2 is induced uniquely in plaque-associated microglia. A genetic variant of PLCG2, PLCG2P522R, is a mild hypermorph that attenuates AD risk. Here, we identified a loss-of-function PLCG2 variant, PLCG2M28L, that confers an increased AD risk. PLCG2P522R attenuated disease in an amyloidogenic murine AD model, whereas PLCG2M28L exacerbated the plaque burden associated with altered phagocytosis and Aβ clearance. The variants bidirectionally modulated disease pathology by inducing distinct transcriptional programs that identified microglial subpopulations associated with protective or detrimental phenotypes. These findings identify PLCG2M28L as a potential AD risk variant and demonstrate that PLCG2 variants can differentially orchestrate microglial responses in AD pathogenesis that can be therapeutically targeted.
Graphical abstract
Tsai, Andy P.; Dong, Chuanpeng; Lin, Peter Bor-Chian, et al. (2023)
Genetic variants of phospholipase C-γ2 alter the phenotype and function of microglia and confer differential risk for Alzheimer’s disease
Immunity; 10.1016/j.immuni.2023.08.008
Copyright: © 2023 The authors.
Published by Elsevier. Open access
Reprinted under a Creative Commons Attribution 4.0 International license (CC BY 4.0)
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