Head Injury and the Risk of Alzheimer's Disease: A Case Control Study

Salib, Emad; Hillier, V.

doi:10.1002/(sici)1099-1166(199703)12:3<363::aid-gps515>3.0.co;2-f

Cited by 77 publications

(38 citation statements)

References 9 publications

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“…A prior history of TBI has been reported to increase the incidence of Alzheimer disease (AD) and other dementias [1][2][3][4][5][6][7], including younger onset dementias [8]. Since the 1920s, repeated mild TBI (mTBI) in boxers has been linked to later onset neuropsychiatric symptoms and signs.…”

Section: Introductionsupporting

confidence: 88%

Chronic Neurodegeneration After Traumatic Brain Injury: Alzheimer Disease, Chronic Traumatic Encephalopathy, or Persistent Neuroinflammation?

2015

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It has long been suggested that prior traumatic brain injury (TBI) increases the subsequent incidence of chronic neurodegenerative disorders, including Alzheimer disease, Parkinson disease, and amyotrophic lateral sclerosis. Among these, the association with Alzheimer disease has the strongest support. There is also a long-recognized association between repeated concussive insults and progressive cognitive decline or other neuropsychiatric abnormalities. The latter was first described in boxers as dementia pugilistica, and has received widespread recent attention in contact sports such as professional American football. The term chronic traumatic encephalopathy was coined to attempt to define a "specific" entity marked by neurobehavioral changes and the extensive deposition of phosphorylated tau protein. Nearly lost in the discussions of post-traumatic neurodegeneration after traumatic brain injury has been the role of sustained neuroinflammation, even though this association has been well established pathologically since the 1950s, and is strongly supported by subsequent preclinical and clinical studies. Manifested by extensive microglial and astroglial activation, such chronic traumatic brain inflammation may be the most important cause of post-traumatic neurodegeneration in terms of prevalence. Critically, emerging preclinical studies indicate that persistent neuroinflammation and associated neurodegeneration may be treatable long after the initiating insult(s).

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Section: Introductionsupporting

confidence: 88%

Chronic Neurodegeneration After Traumatic Brain Injury: Alzheimer Disease, Chronic Traumatic Encephalopathy, or Persistent Neuroinflammation?

2015

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“…2,4,5,9,14,19,21,22,28,33,34 Given the increased risk for AD noted in Apo-E4-expressing patients, the increased likelihood for amyloid plaque deposition in APOE ε4 carriers with TBI supports the reported link between severe TBI and AD. 4,7,9,14,19,22,25,27,28,[31][32][33][34] Initially, we hypothesized that only Apo-E4 expressers would accumulate amyloid in the brain after TBI. Unfortunately, due to our limited sample size, we were unable to test our hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Evidence of increased brain amyloid in severe TBI survivors at 1, 12, and 24 months after injury: report of 2 cases

Gatson

Stebbins²,

Mathews

et al. 2016

JNS

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Traumatic brain injury (TBI) is a major risk factor for Alzheimer’s disease. With respect to amyloid deposition, there are no published serial data regarding the deposition rate of amyloid throughout the brain after TBI. The authors conducted serial 18F-AV-45 (florbetapir F18) positron emission tomography (PET) imaging in 2 patients with severe TBI at 1, 12, and 24 months after injury. A total of 12 brain regions were surveyed for changes in amyloid levels. Case 1 involved a 50-year-old man who experienced a severe TBI. Compared with the 1-month time point, of the 12 brain regions that were surveyed, a decrease in amyloid (as indicated by standard uptake value ratios) was only observed in the hippocampus (−16%, left; −12%, right) and caudate nucleus (−18%, left; −18%, right), suggesting that initial amyloid accumulation in the brain was cleared between time points 1 and 12 months after injury. Compared to the scan at 1 year, a greater increase in amyloid (+15%) was observed in the right hippocampus at the 24-month time point. The patient in Case 2 was a 37-year-old man who suffered severe trauma to the head and a subsequent stroke; he had poor cognitive/functional outcomes and underwent 1.5 years of rehabilitation. Due to a large infarct area on the injured side of the brain (right side), the authors focused primarily on brain regions affected within the left hemisphere. Compared with the 1-month scan, they only found an increase in brain amyloid within the left anterior putamen (+11%) at 12 months after injury. In contrast, decreased amyloid burden was detected in the left caudate nucleus (−48%), occipital cortex (−21%), and precuneus (−19%) brain regions at the 12-month time point, which is indicative of early accumulation and subsequent clearance. In comparison with 12-month values, more clearance was observed, since a reduction in amyloid was found at 24 months after trauma within the left anterior putamen (−12%) and occipital cortex (−15%). Also, by 24 months, most of the amyloid had been cleared and the patient demonstrated improved results on the Rivermead symptom questionnaire, Glasgow Outcome Scale-Extended, and Disability Rating Scale. With respect to APOE status, the patient in Case 1 had two ε3 alleles and the patient in Case 2 had one ε2 and one ε3 allele. In comparison to the findings of the initial scan at 1 month after TBI, by 12 and 24 months after injury amyloid was cleared in some brain regions and increased in others. Serial imaging conducted here suggests that florbetapir F18 PET imaging may be useful in monitoring amyloid dynamics within specific brain regions following severe TBI and may be predictive of cognitive deficits.

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“…A case-controlled study showed that a history of head trauma was significant for both AD and non-AD dementias, but the effect was limited to males (119). Several epidemiologic studies have reported increased risk of dementia in individuals with head trauma (103,145).…”

Section: Chemical and Physical Environmental Exposures And Dementiamentioning

confidence: 99%

Can Dementia Be Prevented? Brain Aging in a Population-Based Context

Haan

Wallace

2004

Annu. Rev. Public Health

146

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s Abstract As a consequence of global aging of the human population, the occurrence of cognitive impairment and dementia is rapidly becoming a significant burden for medical care and public health systems. By the year 2020, the WHO predicts there will be nearly 29 million demented people in both developed and developing countries. Primary and secondary prevention of dementia through individual and population-level interventions could reduce this imminent risk. Vascular risk factors such as type 2 diabetes, hypertension, dietary fat intake, high cholesterol, and obesity have emerged as important influences on the risk of both vascular and Alzheimer's dementia. Understanding the reasons for differences between populations in genetic vulnerability and environmental exposures may help to identify modifiable risk factors that may lead to effective prevention of vascular and Alzheimer's dementia.

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Head Injury and the Risk of Alzheimer's Disease: A Case Control Study

Cited by 77 publications

References 9 publications

Chronic Neurodegeneration After Traumatic Brain Injury: Alzheimer Disease, Chronic Traumatic Encephalopathy, or Persistent Neuroinflammation?

Chronic Neurodegeneration After Traumatic Brain Injury: Alzheimer Disease, Chronic Traumatic Encephalopathy, or Persistent Neuroinflammation?

Evidence of increased brain amyloid in severe TBI survivors at 1, 12, and 24 months after injury: report of 2 cases

Can Dementia Be Prevented? Brain Aging in a Population-Based Context

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