Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice

Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) –initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD m...

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Published inBlood Vol. 129; no. 18; pp. 2547 - 2556
Main Authors Chen, Zu-Lin, Revenko, Alexey S., Singh, Pradeep, MacLeod, A.Robert, Norris, Erin H., Strickland, Sidney
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 04.05.2017
American Society of Hematology
Subjects
Alzheimer Disease - blood
Alzheimer Disease - genetics
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Animals
Brain - blood supply
Brain - metabolism
Brain - pathology
Brain - physiopathology
Cognitive Dysfunction - blood
Cognitive Dysfunction - genetics
Cognitive Dysfunction - pathology
Cognitive Dysfunction - physiopathology
Factor XII - metabolism
Kininogen, High-Molecular-Weight - blood
Mice
Mice, Transgenic
Thrombosis and Hemostasis
Vascular Diseases - blood
Vascular Diseases - genetics
Vascular Diseases - pathology
Vascular Diseases - physiopathology
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Abstract Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) –initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD mice. We have investigated the role of the contact system in AD pathogenesis. Cleavage of high-molecular-weight kininogen (HK), a marker for activation of the inflammatory arm of the contact system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the onset of brain inflammation. Depletion of FXII in AD mice inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brain. Moreover, FXII-depleted AD mice showed better cognitive function than untreated AD mice. These results indicate that FXII-mediated contact system activation contributes to AD pathogenesis, and therefore this system may offer novel targets for AD treatment. •The plasma contact system is activated early in AD mice and temporally correlated with the onset of brain inflammation.•Depletion of contact system initiator FXII ameliorates brain pathology and cognitive impairment in AD mice.
AbstractList Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) -initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD mice. We have investigated the role of the contact system in AD pathogenesis. Cleavage of high-molecular-weight kininogen (HK), a marker for activation of the inflammatory arm of the contact system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the onset of brain inflammation. Depletion of FXII in AD mice inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brain. Moreover, FXII-depleted AD mice showed better cognitive function than untreated AD mice. These results indicate that FXII-mediated contact system activation contributes to AD pathogenesis, and therefore this system may offer novel targets for AD treatment.
Publisher's Note: There is an Inside Blood Commentary on this article in this issue. The plasma contact system is activated early in AD mice and temporally correlated with the onset of brain inflammation. Depletion of contact system initiator FXII ameliorates brain pathology and cognitive impairment in AD mice. Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) –initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD mice. We have investigated the role of the contact system in AD pathogenesis. Cleavage of high-molecular-weight kininogen (HK), a marker for activation of the inflammatory arm of the contact system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the onset of brain inflammation. Depletion of FXII in AD mice inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brain. Moreover, FXII-depleted AD mice showed better cognitive function than untreated AD mice. These results indicate that FXII-mediated contact system activation contributes to AD pathogenesis, and therefore this system may offer novel targets for AD treatment.
Key Points The plasma contact system is activated early in AD mice and temporally correlated with the onset of brain inflammation. Depletion of contact system initiator FXII ameliorates brain pathology and cognitive impairment in AD mice.
Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear. The factor XII (FXII) –initiated contact system can trigger both vascular pathology and inflammation and is activated in AD patients and AD mice. We have investigated the role of the contact system in AD pathogenesis. Cleavage of high-molecular-weight kininogen (HK), a marker for activation of the inflammatory arm of the contact system, is increased in a mouse model of AD, and this cleavage is temporally correlated with the onset of brain inflammation. Depletion of FXII in AD mice inhibited HK cleavage in plasma and reduced neuroinflammation, fibrinogen deposition, and neurodegeneration in the brain. Moreover, FXII-depleted AD mice showed better cognitive function than untreated AD mice. These results indicate that FXII-mediated contact system activation contributes to AD pathogenesis, and therefore this system may offer novel targets for AD treatment. •The plasma contact system is activated early in AD mice and temporally correlated with the onset of brain inflammation.•Depletion of contact system initiator FXII ameliorates brain pathology and cognitive impairment in AD mice.
Author Singh, Pradeep
Norris, Erin H.
Strickland, Sidney
Chen, Zu-Lin
MacLeod, A.Robert
Revenko, Alexey S.
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  givenname: Alexey S.
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  surname: MacLeod
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  organization: Department of Antisense Drug Discovery, Ionis Pharmaceuticals, Inc., Carlsbad, CA
– sequence: 5
  givenname: Erin H.
  surname: Norris
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  email: strickland@rockefeller.edu
  organization: Patricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, New York, NY
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SSID ssj0014325
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Snippet Vascular abnormalities and inflammation are found in many Alzheimer disease (AD) patients, but whether these changes play a causative role in AD is not clear....
Key Points The plasma contact system is activated early in AD mice and temporally correlated with the onset of brain inflammation. Depletion of contact system...
Publisher's Note: There is an Inside Blood Commentary on this article in this issue. The plasma contact system is activated early in AD mice and temporally...
SourceID pubmedcentral
proquest
crossref
pubmed
elsevier
SourceType Open Access Repository
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Index Database
Publisher
StartPage 2547
SubjectTerms Alzheimer Disease - blood
Alzheimer Disease - genetics
Alzheimer Disease - pathology
Alzheimer Disease - physiopathology
Animals
Brain - blood supply
Brain - metabolism
Brain - pathology
Brain - physiopathology
Cognitive Dysfunction - blood
Cognitive Dysfunction - genetics
Cognitive Dysfunction - pathology
Cognitive Dysfunction - physiopathology
Factor XII - metabolism
Kininogen, High-Molecular-Weight - blood
Mice
Mice, Transgenic
Thrombosis and Hemostasis
Vascular Diseases - blood
Vascular Diseases - genetics
Vascular Diseases - pathology
Vascular Diseases - physiopathology
Title Depletion of coagulation factor XII ameliorates brain pathology and cognitive impairment in Alzheimer disease mice
URI https://dx.doi.org/10.1182/blood-2016-11-753202
https://www.ncbi.nlm.nih.gov/pubmed/28242605
https://search.proquest.com/docview/1872871430
https://pubmed.ncbi.nlm.nih.gov/PMC5418637
Volume 129
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