Microglial neuroinflammation contributes to tau accumulation in chronic traumatic encephalopathy

The chronic effects of repetitive head impacts (RHI) on the development of neuroinflammation and its relationship to chronic traumatic encephalopathy (CTE) are unknown. Here we set out to determine the relationship between RHI exposure, neuroinflammation, and the development of hyperphosphorylated t...

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Bibliographic Details
Published in:Acta neuropathologica communications 2016-10, Vol.4 (1), p.112-112, Article 112
Main Authors: Cherry, Jonathan D, Tripodis, Yorghos, Alvarez, Victor E, Huber, Bertrand, Kiernan, Patrick T, Daneshvar, Daniel H, Mez, Jesse, Montenigro, Philip H, Solomon, Todd M, Alosco, Michael L, Stern, Robert A, McKee, Ann C, Stein, Thor D
Format: Article
Language:English
Subjects:
Adult
Age Factors
Aged
Antigens, CD - metabolism
Antigens, Differentiation, Myelomonocytic - metabolism
Athletes
Athletic Injuries - complications
Athletic Injuries - immunology
Athletic Injuries - pathology
Brain
Cell Count
Chronic Traumatic Encephalopathy - etiology
Chronic Traumatic Encephalopathy - immunology
Chronic Traumatic Encephalopathy - pathology
Cohort Studies
Concussion
Encephalitis - etiology
Encephalitis - immunology
Encephalitis - pathology
Encephalopathy
Football
Football - injuries
Frontal Lobe - immunology
Frontal Lobe - pathology
Humans
Male
Medical research
Medicine, Experimental
Microglia - immunology
Microglia - pathology
Nervous system diseases
Regression Analysis
Severity of Illness Index
tau Proteins - metabolism
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Summary:The chronic effects of repetitive head impacts (RHI) on the development of neuroinflammation and its relationship to chronic traumatic encephalopathy (CTE) are unknown. Here we set out to determine the relationship between RHI exposure, neuroinflammation, and the development of hyperphosphorylated tau (ptau) pathology and dementia risk in CTE. We studied a cohort of 66 deceased American football athletes from the Boston University-Veteran's Affairs-Concussion Legacy Foundation Brain Bank as well as 16 non-athlete controls. Subjects with a neurodegenerative disease other than CTE were excluded. Counts of total and activated microglia, astrocytes, and ptau pathology were performed in the dorsolateral frontal cortex (DLF). Binary logistic and simultaneous equation regression models were used to test associations between RHI exposure, microglia, ptau pathology, and dementia. Duration of RHI exposure and the development and severity of CTE were associated with reactive microglial morphology and increased numbers of CD68 immunoreactive microglia in the DLF. A simultaneous equation regression model demonstrated that RHI exposure had a significant direct effect on CD68 cell density (p 
ISSN:2051-5960
2051-5960
DOI:10.1186/s40478-016-0382-8