Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer’s disease pathology

The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD) 1 . Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, L...

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Published inNature aging Vol. 2; no. 12; pp. 1138 - 1144
Main Authors Pereira, Joana B., Janelidze, Shorena, Strandberg, Olof, Whelan, Christopher D., Zetterberg, Henrik, Blennow, Kaj, Palmqvist, Sebastian, Stomrud, Erik, Mattsson-Carlgren, Niklas, Hansson, Oskar
Format Journal Article
LanguageEnglish
Published United States Nature Publishing Group 01.12.2022
Nature Publishing Group US
Subjects
Alzheimer Disease - pathology
Alzheimer's disease
Amyloid
Amyloidogenic Proteins
Basic Medicine
c-Mer Tyrosine Kinase
Cognitive Dysfunction - pathology
Humans
Letter
Medical and Health Sciences
Medicin och hälsovetenskap
Medicinska och farmaceutiska grundvetenskaper
Microglia - pathology
Neurosciences
Neurovetenskaper
Pathology
tau Proteins
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Abstract The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD) 1 . Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A + ), 64 with additional evidence of tau-PET pathology (A + T + ) and 159 without amyloid- or tau-PET pathology (A − T − ). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A + individuals in addition to slower tau deposition and cognitive decline in A + T + subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A + T + group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD.
AbstractList The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD) 1 . Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A + ), 64 with additional evidence of tau-PET pathology (A + T + ) and 159 without amyloid- or tau-PET pathology (A − T − ). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A + individuals in addition to slower tau deposition and cognitive decline in A + T + subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A + T + group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD.
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD)1. Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A+), 64 with additional evidence of tau-PET pathology (A+T+) and 159 without amyloid- or tau-PET pathology (A−T−). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A+ individuals in addition to slower tau deposition and cognitive decline in A+T+ subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A+T+ group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD.
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD)1. Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A+), 64 with additional evidence of tau-PET pathology (A+T+) and 159 without amyloid- or tau-PET pathology (A-T-). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A+ individuals in addition to slower tau deposition and cognitive decline in A+T+ subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A+T+ group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD.The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD)1. Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A+), 64 with additional evidence of tau-PET pathology (A+T+) and 159 without amyloid- or tau-PET pathology (A-T-). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A+ individuals in addition to slower tau deposition and cognitive decline in A+T+ subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A+T+ group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD.
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD) . Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A ), 64 with additional evidence of tau-PET pathology (A T ) and 159 without amyloid- or tau-PET pathology (A T ). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A individuals in addition to slower tau deposition and cognitive decline in A T subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A T group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD.
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD) 1 . Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A + ), 64 with additional evidence of tau-PET pathology (A + T + ) and 159 without amyloid- or tau-PET pathology (A − T − ). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A + individuals in addition to slower tau deposition and cognitive decline in A + T + subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A + T + group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD. The authors show that higher concentrations of disease-associated microglial activation stage 2 (DAM2) markers are associated with reduced tau accumulation and slower cognitive decline in nondemented individuals at risk for developing Alzheimer’s disease, suggesting that microglial activation delays disease progression.
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD)1. Here, we measured the microglial marker soluble TREM2 and the disease-associated microglial activation stage 2 markers AXL, MERTK, GAS6, LPL, CST7, SPP1 and CSF1 in nondemented individuals from the Swedish BioFINDER-2 cohort who underwent longitudinal tau-positron emission tomography (PET), amyloid-PET and global cognitive assessment. To assess whether baseline microglial markers had an effect on AD-related changes, we studied three sub-groups of individuals: 121 with evidence of amyloid-PET pathology (A+), 64 with additional evidence of tau-PET pathology (A+T+) and 159 without amyloid- or tau-PET pathology (A−T−). Our results showed that increased levels of TREM2 were associated with slower amyloid accumulation in A+ individuals in addition to slower tau deposition and cognitive decline in A+T+ subjects. Similarly, higher levels of AXL, MERTK, GAS6, LPL, CST7 and CSF1 predicted slower tau accumulation and/or cognitive decline in the A+T+ group. These findings have important implications for future therapeutic strategies aiming to boost microglial protective functions in AD.The authors show that higher concentrations of disease-associated microglial activation stage 2 (DAM2) markers are associated with reduced tau accumulation and slower cognitive decline in nondemented individuals at risk for developing Alzheimer’s disease, suggesting that microglial activation delays disease progression.
Author Pereira, Joana B.
Janelidze, Shorena
Stomrud, Erik
Whelan, Christopher D.
Zetterberg, Henrik
Blennow, Kaj
Mattsson-Carlgren, Niklas
Strandberg, Olof
Palmqvist, Sebastian
Hansson, Oskar
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Snippet The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD) 1...
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD) ....
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer’s disease (AD)1....
The role of microglia in tau accumulation is currently unclear but could provide an important insight into the mechanisms underlying Alzheimer's disease (AD)1....
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StartPage 1138
SubjectTerms Alzheimer Disease - pathology
Alzheimer's disease
Amyloid
Amyloidogenic Proteins
Basic Medicine
c-Mer Tyrosine Kinase
Cognitive Dysfunction - pathology
Humans
Letter
Medical and Health Sciences
Medicin och hälsovetenskap
Medicinska och farmaceutiska grundvetenskaper
Microglia - pathology
Neurosciences
Neurovetenskaper
Pathology
tau Proteins
Title Microglial activation protects against accumulation of tau aggregates in nondemented individuals with underlying Alzheimer’s disease pathology
URI https://www.ncbi.nlm.nih.gov/pubmed/37118533
https://www.proquest.com/docview/3102044288
https://www.proquest.com/docview/2807918471
https://pubmed.ncbi.nlm.nih.gov/PMC10154192
https://gup.ub.gu.se/publication/323601
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