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Summary: Researchers report microglia may actually protect the brain against Alzheimer’s disease by containing the spread of amyloid plaques.
Clusters of immune cells in the brain previously associated with Alzheimer’s actually protect against the disease by containing the spread of damaging amyloid plaques, a new Yale University School of Medicine study shows.
The findings, published online May 18 in the journal Neuron, are further evidence that inflammation byproducts of these immune cells are probably not a major culprit in Alzheimer’s, as previously suspected, said the researchers.
“It suggests we should be enhancing the function of these immune cells, not trying to suppress it,” said Jaime Grutzendler, associate professor of neurology and neuroscience and senior author of the study.
Large numbers of immune system cells called microglia are found around amyloid plaques, which are the hallmark of Alzheimer’s disease. Some theorized that the toxins released by microglia trying to attack the plaques contributed to damage in surrounding brain cells.
Using a mouse model of Alzheimer’s, Grutzendler and lead authors Peng Yuan and Carlo Condello studied a rare genetic mutation of the gene TREM2 that blocks ability of microglia to respond to threats to the brain. They found that plaques in mice with this mutation were covered with spiky fibers projecting outward in the brain. TREM2 and its human equivalent, which in mutated form increases risk of Alzheimer’s, appear to be crucial to allowing microglia to corral and contain amyloid plaques, thereby limiting their damage, said the scientists.
“The cells act as a physical barrier that prevents outward expansion of plaques and, therefore, makes them less toxic to the connections between surrounding brain cells,” Grutzendler said.
Differences in the ability of microglia to corral plaques may help explain why some individuals with large amount of amyloid plaques never develop the cognitive deficits associated with Alzheimer’s. Instead, in other individuals, the process of aging may make microglia ineffective at containing these plaques, thereby contributing to loss of memory and cognitive abilities characteristic of Alzheimer’s, Grutzendler suggests.
[divider]About this Alzheimer’s research article[/divider]
Researchers from the University of Washington and Washington University also contributed to the research.
Funding: Funding information not available.
Source: Bill Hathaway – Yale Image Source: This NeuroscienceNews.com image is credited to the researchers/Yale. Original Research: Abstract for “TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy” by Peng Yuan, Carlo Condello, C. Dirk Keene, Yaming Wang, Thomas D. Bird, Steven M. Paul, Wenjie Luo, Marco Colonna, David Baddeley, and Jaime Grutzendler in Cell Reports. Published online May 18 2016 doi:10.1016/j.neuron.2016.05.003
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[cbtabs][cbtab title=”MLA”]Yale. “Immune Cells May Protect Against Alzheimer’s.” NeuroscienceNews. NeuroscienceNews, 19 May 2016. <https://neurosciencenews.com/microglia-alzheimers-neurology-4254/>.[/cbtab][cbtab title=”APA”]Yale. (2016, May 19). Immune Cells May Protect Against Alzheimer’s. NeuroscienceNews. Retrieved May 19, 2016 from https://neurosciencenews.com/microglia-alzheimers-neurology-4254/[/cbtab][cbtab title=”Chicago”]Yale. “Immune Cells May Protect Against Alzheimer’s.” NeuroscienceNews. https://neurosciencenews.com/microglia-alzheimers-neurology-4254/ (accessed May 19, 2016).[/cbtab][/cbtabs]
TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy
Highlights •TREM2/DAP12 signaling regulates microglia process envelopment of amyloid plaques •Loss of microglia envelopment in TREM2/DAP12 deficiency reduces plaque compaction •STORM microscopy shows greater fibril branching and surface area in TREM2 deficiency •Human R47H TREM2 variant impairs the microglia barrier and worsens axonal dystrophy
Summary Haplodeficiency of the microglia gene TREM2 increases risk for late-onset Alzheimer’s disease (AD) but the mechanisms remain uncertain. To investigate this, we used high-resolution confocal and super-resolution (STORM) microscopy in AD-like mice and human AD tissue. We found that microglia processes, rich in TREM2, tightly surround early amyloid fibrils and plaques promoting their compaction and insulation. In Trem2- or DAP12-haplodeficient mice and in humans with R47H TREM2 mutations, microglia had a markedly reduced ability to envelop amyloid deposits. This led to an increase in less compact plaques with longer and branched amyloid fibrils resulting in greater surface exposure to adjacent neurites. This was associated with more severe neuritic tau hyperphosphorylation and axonal dystrophy around amyloid deposits. Thus, TREM2 deficiency may disrupt the formation of a neuroprotective microglia barrier that regulates amyloid compaction and insulation. Pharmacological modulation of this barrier could be a novel therapeutic strategy for AD.
“TREM2 Haplodeficiency in Mice and Humans Impairs the Microglia Barrier Function Leading to Decreased Amyloid Compaction and Severe Axonal Dystrophy” by Peng Yuan, Carlo Condello, C. Dirk Keene, Yaming Wang, Thomas D. Bird, Steven M. Paul, Wenjie Luo, Marco Colonna, David Baddeley, and Jaime Grutzendler in Cell Reports. Published online May 18 2016 doi:10.1016/j.neuron.2016.05.003
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