Iron loading is a prominent feature of activated microglia in Alzheimer’s disease patients

Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as inc...

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Vydané v:Acta neuropathologica communications Ročník 9; číslo 1; s. 27 - 15
Hlavní autori: Kenkhuis, Boyd, Somarakis, Antonios, de Haan, Lorraine, Dzyubachyk, Oleh, IJsselsteijn, Marieke E., de Miranda, Noel F. C. C., Lelieveldt, Boudewijn P. F., Dijkstra, Jouke, van Roon-Mom, Willeke M. C., Höllt, Thomas, van der Weerd, Louise
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London BioMed Central 17.02.2021
BioMed Central Ltd
Nature Publishing Group
BMC
Predmet:
Alzheimer
Alzheimer's disease
Antibodies
Antigens
Binding sites
Biomedical and Life Sciences
Biomedicine
Development and progression
Ferritin
Histology
Human
Iron
Microglia
Neurology
Neurosciences
Pathology
Netherlands
Human
Iron
Alzheimer
Ferritin
Microglia
ISSN:2051-5960, 2051-5960
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Abstract Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL + Iba1 + -microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL + Iba1 + -microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.
AbstractList Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL + Iba1 + -microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL + Iba1 + -microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.
Brain iron accumulation has been found to accelerate disease progression in amyloid-[beta](A[beta]) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL.sup.+Iba1.sup.+-microglia, which were found to be the predominant A[beta]-plaque infiltrating microglia. Finally, an increase of FTL.sup.+Iba1.sup.+-microglia was seen in patients with high A[beta] load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with A[beta].
Brain iron accumulation has been found to accelerate disease progression in amyloid-[beta](A[beta]) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL.sup.+Iba1.sup.+-microglia, which were found to be the predominant A[beta]-plaque infiltrating microglia. Finally, an increase of FTL.sup.+Iba1.sup.+-microglia was seen in patients with high A[beta] load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with A[beta]. Keywords: Alzheimer, Microglia, Iron, Ferritin, Human
Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL+Iba1+-microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL+Iba1+-microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.
Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL+Iba1+-microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL+Iba1+-microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.
Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL+Iba1+-microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL+Iba1+-microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL+Iba1+-microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL+Iba1+-microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.
Abstract Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL+Iba1+-microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL+Iba1+-microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.
Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown. Microglia have been identified as key players in the disease pathogenesis, and are highly reactive cells responding to aberrations such as increased iron levels. Therefore, using histological methods, multispectral immunofluorescence and an automated in-house developed microglia segmentation and analysis pipeline, we studied the occurrence of iron-accumulating microglia and the effect on its activation state in human Alzheimer brains. We identified a subset of microglia with increased expression of the iron storage protein ferritin light chain (FTL), together with increased Iba1 expression, decreased TMEM119 and P2RY12 expression. This activated microglia subset represented iron-accumulating microglia and appeared morphologically dystrophic. Multispectral immunofluorescence allowed for spatial analysis of FTL Iba1 -microglia, which were found to be the predominant Aβ-plaque infiltrating microglia. Finally, an increase of FTL Iba1 -microglia was seen in patients with high Aβ load and Tau load. These findings suggest iron to be taken up by microglia and to influence the functional phenotype of these cells, especially in conjunction with Aβ.
ArticleNumber 27
Audience Academic
Author de Miranda, Noel F. C. C.
IJsselsteijn, Marieke E.
Dijkstra, Jouke
Dzyubachyk, Oleh
Lelieveldt, Boudewijn P. F.
Höllt, Thomas
Kenkhuis, Boyd
van Roon-Mom, Willeke M. C.
van der Weerd, Louise
Somarakis, Antonios
de Haan, Lorraine
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  orcidid: 0000-0002-4000-6779
  surname: Kenkhuis
  fullname: Kenkhuis, Boyd
  email: b.kenkhuis@lumc.nl
  organization: Department of Human Genetics, Leiden University Medical Center, Department of Radiology, Leiden University Medical Center
– sequence: 2
  givenname: Antonios
  surname: Somarakis
  fullname: Somarakis, Antonios
  organization: Department of Radiology, Leiden University Medical Center
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  surname: de Haan
  fullname: de Haan, Lorraine
  organization: Department of Pathology, Leiden University Medical Center
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  fullname: Dzyubachyk, Oleh
  organization: Department of Radiology, Leiden University Medical Center, Department of Cell and Chemical Biology, Leiden University Medical Center
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  surname: IJsselsteijn
  fullname: IJsselsteijn, Marieke E.
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  fullname: de Miranda, Noel F. C. C.
  organization: Department of Pathology, Leiden University Medical Center
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  givenname: Boudewijn P. F.
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  fullname: Lelieveldt, Boudewijn P. F.
  organization: Department of Radiology, Leiden University Medical Center
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  surname: Dijkstra
  fullname: Dijkstra, Jouke
  organization: Department of Radiology, Leiden University Medical Center
– sequence: 9
  givenname: Willeke M. C.
  surname: van Roon-Mom
  fullname: van Roon-Mom, Willeke M. C.
  organization: Department of Human Genetics, Leiden University Medical Center
– sequence: 10
  givenname: Thomas
  surname: Höllt
  fullname: Höllt, Thomas
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– sequence: 11
  givenname: Louise
  surname: van der Weerd
  fullname: van der Weerd, Louise
  organization: Department of Human Genetics, Leiden University Medical Center, Department of Radiology, Leiden University Medical Center
BackLink https://www.ncbi.nlm.nih.gov/pubmed/33597025$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Human
Iron
Alzheimer
Ferritin
Microglia
Language English
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Snippet Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown....
Brain iron accumulation has been found to accelerate disease progression in amyloid-[beta](A[beta]) positive Alzheimer patients, though the mechanism is still...
Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still unknown....
Abstract Brain iron accumulation has been found to accelerate disease progression in amyloid-β(Aβ) positive Alzheimer patients, though the mechanism is still...
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StartPage 27
SubjectTerms Alzheimer
Alzheimer's disease
Antibodies
Antigens
Binding sites
Biomedical and Life Sciences
Biomedicine
Development and progression
Ferritin
Histology
Human
Iron
Microglia
Neurology
Neurosciences
Pathology
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Title Iron loading is a prominent feature of activated microglia in Alzheimer’s disease patients
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Volume 9
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