Beta-amyloid deposition in chronic traumatic encephalopathy

Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer’s disease (AD). Although tra...

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Published inActa neuropathologica Vol. 130; no. 1; pp. 21 - 34
Main Authors Stein, Thor D., Montenigro, Philip H., Alvarez, Victor E., Xia, Weiming, Crary, John F., Tripodis, Yorghos, Daneshvar, Daniel H., Mez, Jesse, Solomon, Todd, Meng, Gaoyuan, Kubilus, Caroline A., Cormier, Kerry A., Meng, Steven, Babcock, Katharine, Kiernan, Patrick, Murphy, Lauren, Nowinski, Christopher J., Martin, Brett, Dixon, Diane, Stern, Robert A., Cantu, Robert C., Kowall, Neil W., McKee, Ann C.
Format Journal Article
LanguageEnglish
Published Berlin/Heidelberg Springer Berlin Heidelberg 01.07.2015
Springer
Springer Nature B.V
Subjects
Adult
Age Factors
Aged
Aged, 80 and over
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Apolipoprotein E4 - genetics
Athletes
Athletic Injuries - epidemiology
Athletic Injuries - genetics
Athletic Injuries - metabolism
Athletic Injuries - pathology
Brain
Brain - metabolism
Brain - pathology
Brain Injury, Chronic - epidemiology
Brain Injury, Chronic - genetics
Brain Injury, Chronic - metabolism
Brain Injury, Chronic - pathology
Chronic brain injury
Chronic traumatic encephalopathy
Clinical outcomes
Cohort Studies
Comorbidity
Dementia
Diagnosis
Encephalopathy
Humans
Medicine
Medicine & Public Health
Middle Aged
Nervous system diseases
Neurodegenerative Diseases - epidemiology
Neurodegenerative Diseases - genetics
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Neurophysiology
Neurosciences
Neurosurgery
Original Paper
Pathology
Plaque, Amyloid - etiology
Plaque, Amyloid - metabolism
Plaque, Amyloid - pathology
Postconcussional syndrome
Severity of Illness Index
tau Proteins - metabolism
Traumatic brain injury
Veterans
War-Related Injuries - epidemiology
War-Related Injuries - genetics
War-Related Injuries - metabolism
War-Related Injuries - pathology
New York
United States > US
Tau
Chronic traumatic encephalopathy
Alzheimer’s disease
Neurodegenerative disorders
Beta-amyloid
Dementia
Online AccessGet full text

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Abstract Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer’s disease (AD). Although trauma has been suggested to increase amyloid β peptide (Aβ) levels, the extent of Aβ deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE ( n  = 114, mean age at death = 60) to test the hypothesis that Aβ deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Aβ deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Aβ deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p  < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Aβ plaques and those without. Aβ deposition was significantly associated with the presence of the APOE ε4 allele ( p  = 0.035), older age at symptom onset ( p  < 0.001), and older age at death ( p  < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage ( β  = 2.43, p  = 0.018), co-morbid Lewy body disease (OR = 5.01, p  = 0.009), and dementia (OR = 4.45, p  = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both Aβ plaques and total levels of Aβ1-40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that Aβ deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that Aβ is associated with both pathological and clinical progression of CTE independent of age.
AbstractList Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid [beta] peptide (A[beta]) levels, the extent of A[beta] deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that A[beta] deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that A[beta] deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, A[beta] deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with A[beta] plaques and those without. A[beta] deposition was significantly associated with the presence of the APOE [epsilon]4 allele (p = 0.035), older age at symptom onset (p < 0.001), and older age at death (p < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage ([beta] = 2.43, p = 0.018), co-morbid Lewy body disease (OR = 5.01, p = 0.009), and dementia (OR = 4.45, p = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both A[beta] plaques and total levels of A[beta]1-40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that A[beta] deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that A[beta] is associated with both pathological and clinical progression of CTE independent of age. Electronic supplementary material The online version of this article (doi:10.1007/s00401-015-1435-y) contains supplementary material, which is available to authorized users.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer’s disease (AD). Although trauma has been suggested to increase amyloid β peptide (Aβ) levels, the extent of Aβ deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE ( n  = 114, mean age at death = 60) to test the hypothesis that Aβ deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Aβ deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Aβ deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p  < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Aβ plaques and those without. Aβ deposition was significantly associated with the presence of the APOE ε4 allele ( p  = 0.035), older age at symptom onset ( p  < 0.001), and older age at death ( p  < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage ( β  = 2.43, p  = 0.018), co-morbid Lewy body disease (OR = 5.01, p  = 0.009), and dementia (OR = 4.45, p  = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both Aβ plaques and total levels of Aβ1-40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that Aβ deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that Aβ is associated with both pathological and clinical progression of CTE independent of age.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer’s disease (AD). Although trauma has been suggested to increase amyloid β peptide (Aβ) levels, the extent of Aβ deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE ( n = 114, mean age at death = 60) to test the hypothesis that Aβ deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Aβ deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Aβ deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Aβ plaques and those without. Aβ deposition was significantly associated with the presence of the APOE ε4 allele ( p = 0.035), older age at symptom onset ( p < 0.001), and older age at death ( p < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (β = 2.43, p = 0.018), co-morbid Lewy body disease (OR = 5.01, p = 0.009), and dementia (OR = 4.45, p = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both Aβ plaques and total levels of Aβ1–40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that Aβ deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that Aβ is associated with both pathological and clinical progression of CTE independent of age.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid [beta] peptide (A[beta]) levels, the extent of A[beta] deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that A[beta] deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that A[beta] deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, A[beta] deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with A[beta] plaques and those without. A[beta] deposition was significantly associated with the presence of the APOE [straight epsilon]4 allele (p = 0.035), older age at symptom onset (p < 0.001), and older age at death (p < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage ([beta] = 2.43, p = 0.018), co-morbid Lewy body disease (OR = 5.01, p = 0.009), and dementia (OR = 4.45, p = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both A[beta] plaques and total levels of A[beta]1-40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that A[beta] deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that A[beta] is associated with both pathological and clinical progression of CTE independent of age.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid β peptide (Aβ) levels, the extent of Aβ deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that Aβ deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that Aβ deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, Aβ deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with Aβ plaques and those without. Aβ deposition was significantly associated with the presence of the APOE ε4 allele (p = 0.035), older age at symptom onset (p < 0.001), and older age at death (p < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage (β = 2.43, p = 0.018), co-morbid Lewy body disease (OR = 5.01, p = 0.009), and dementia (OR = 4.45, p = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both Aβ plaques and total levels of Aβ1-40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that Aβ deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that Aβ is associated with both pathological and clinical progression of CTE independent of age.
Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by the abnormal accumulation of tau in a unique pattern that is distinct from other tauopathies, including Alzheimer's disease (AD). Although trauma has been suggested to increase amyloid [beta] peptide (A[beta]) levels, the extent of A[beta] deposition in CTE has not been thoroughly characterized. We studied a heterogeneous cohort of deceased athletes and military veterans with neuropathologically diagnosed CTE (n = 114, mean age at death = 60) to test the hypothesis that A[beta] deposition is altered in CTE and associated with more severe pathology and worse clinical outcomes. We found that A[beta] deposition, either as diffuse or neuritic plaques, was present in 52 % of CTE subjects. Moreover, A[beta] deposition in CTE occurred at an accelerated rate and with altered dynamics in CTE compared to a normal aging population (OR = 3.8, p < 0.001). We also found a clear pathological and clinical dichotomy between those CTE cases with A[beta] plaques and those without. A[beta] deposition was significantly associated with the presence of the APOE [epsilon]4 allele (p = 0.035), older age at symptom onset (p < 0.001), and older age at death (p < 0.001). In addition, when controlling for age, neuritic plaques were significantly associated with increased CTE tauopathy stage ([beta] = 2.43, p = 0.018), co-morbid Lewy body disease (OR = 5.01, p = 0.009), and dementia (OR = 4.45, p = 0.012). A subset of subjects met the diagnostic criteria for both CTE and AD, and in these subjects both A[beta] plaques and total levels of A[beta]1-40 were increased at the depths of the cortical sulcus compared to the gyral crests. Overall, these findings suggest that A[beta] deposition is altered and accelerated in a cohort of CTE subjects compared to normal aging and that A[beta] is associated with both pathological and clinical progression of CTE independent of age.
Audience Academic
Author Stein, Thor D.
Xia, Weiming
Mez, Jesse
Tripodis, Yorghos
Kiernan, Patrick
Daneshvar, Daniel H.
Martin, Brett
Babcock, Katharine
Cantu, Robert C.
Alvarez, Victor E.
Murphy, Lauren
McKee, Ann C.
Meng, Steven
Solomon, Todd
Cormier, Kerry A.
Nowinski, Christopher J.
Meng, Gaoyuan
Dixon, Diane
Kowall, Neil W.
Montenigro, Philip H.
Crary, John F.
Kubilus, Caroline A.
Stern, Robert A.
AuthorAffiliation 6 Department of Neurology, Boston University School of Medicine, Boston, MA 02118, USA
8 Fishberg Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
10 Department of Biostatistics, Boston University School of Medicine, Boston, MA 02118, USA
13 Department of Neurosurgery, Boston University School of Medicine, Boston, MA 02118, USA
12 Sports Legacy Institute, Waltham, MA 02451, USA
5 Department of Anatomy and Neurobiology, Boston University School of Medicine, Boston, MA 02118, USA
4 Department of Pathology and Laboratory Medicine, Boston University School of Medicine, Boston, MA 02118, USA
2 Department of Veterans Affairs Medical Center, Bedford, MA 01730, USA
14 Department of Neurosurgery, Emerson Hospital, Concord, MA 01742, USA
7 Department of Pathology, Icahn School of Medicine at Mount Sinai, New York, NY 10029, USA
1 VA Boston Healthcare System, Boston, MA 02130, USA
9 The Ronald M. Loeb Center for Alzheimer’s Disease, Icahn School of Medicine at Mou
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– name: 2 Department of Veterans Affairs Medical Center, Bedford, MA 01730, USA
– name: 3 Alzheimer’s Disease Center, Boston University School of Medicine, Boston, MA 02118, USA
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/25943889$$D View this record in MEDLINE/PubMed
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Masliah, Rockenstein, Veinbergs (CR25) 2001; 98
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Snippet Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease associated with repetitive mild traumatic brain injury. It is defined pathologically by...
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StartPage 21
SubjectTerms Adult
Age Factors
Aged
Aged, 80 and over
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Apolipoprotein E4 - genetics
Athletes
Athletic Injuries - epidemiology
Athletic Injuries - genetics
Athletic Injuries - metabolism
Athletic Injuries - pathology
Brain
Brain - metabolism
Brain - pathology
Brain Injury, Chronic - epidemiology
Brain Injury, Chronic - genetics
Brain Injury, Chronic - metabolism
Brain Injury, Chronic - pathology
Chronic brain injury
Chronic traumatic encephalopathy
Clinical outcomes
Cohort Studies
Comorbidity
Dementia
Diagnosis
Encephalopathy
Humans
Medicine
Medicine & Public Health
Middle Aged
Nervous system diseases
Neurodegenerative Diseases - epidemiology
Neurodegenerative Diseases - genetics
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Neurophysiology
Neurosciences
Neurosurgery
Original Paper
Pathology
Plaque, Amyloid - etiology
Plaque, Amyloid - metabolism
Plaque, Amyloid - pathology
Postconcussional syndrome
Severity of Illness Index
tau Proteins - metabolism
Traumatic brain injury
Veterans
War-Related Injuries - epidemiology
War-Related Injuries - genetics
War-Related Injuries - metabolism
War-Related Injuries - pathology
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Title Beta-amyloid deposition in chronic traumatic encephalopathy
URI https://link.springer.com/article/10.1007/s00401-015-1435-y
https://www.ncbi.nlm.nih.gov/pubmed/25943889
https://www.proquest.com/docview/1699213458
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https://pubmed.ncbi.nlm.nih.gov/PMC4529056
Volume 130
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