Association of traumatic brain injury with dementia and memory decline in older adults in the United States

Grasset, Leslie; Glymour, M. Maria; Yaffe, Kristine; Swift, Samuel L.; Gianattasio, Kan Z.; Power, Melinda C.; Hazzouri, Adina Zeki Al

doi:10.1002/alz.12080

Cited by 30 publications

(15 citation statements)

References 46 publications

(147 reference statements)

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“…According to the United States CDC, TBI can be caused by a bump, blow, or jolt inflicted to the head or by a penetrating head injury that will cause a disruption of the normal brain function and will have short- and long-term effects on health [ 687 , 688 ]. TBI is considered as one of the risk factors for the development of AD and it is associated with an earlier dementia onset [ 689 – 691 ]. The recovery rates among people that have suffered TBI differ among individuals, and multiple metanalyses point out a relationship between the APOE4 genotype and increased risk of poor long-term outcomes following TBI [ 692 , 693 ].…”

Section: Implications Of Apoe In Other Neurodegene...mentioning

confidence: 99%

APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer’s disease pathology and brain diseases

Fernández-Calle

Konings

Frontiñán-Rubio

et al. 2022

Mol Neurodegeneration

114

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ApoE is the major lipid and cholesterol carrier in the CNS. There are three major human polymorphisms, apoE2, apoE3, and apoE4, and the genetic expression of APOE4 is one of the most influential risk factors for the development of late-onset Alzheimer's disease (AD). Neuroinflammation has become the third hallmark of AD, together with Amyloid-β plaques and neurofibrillary tangles of hyperphosphorylated aggregated tau protein. This review aims to broadly and extensively describe the differential aspects concerning apoE. Starting from the evolution of apoE to how APOE's single-nucleotide polymorphisms affect its structure, function, and involvement during health and disease. This review reflects on how APOE's polymorphisms impact critical aspects of AD pathology, such as the neuroinflammatory response, particularly the effect of APOE on astrocytic and microglial function and microglial dynamics, synaptic function, amyloid-β load, tau pathology, autophagy, and cell–cell communication. We discuss influential factors affecting AD pathology combined with the APOE genotype, such as sex, age, diet, physical exercise, current therapies and clinical trials in the AD field. The impact of the APOE genotype in other neurodegenerative diseases characterized by overt inflammation, e.g., alpha- synucleinopathies and Parkinson's disease, traumatic brain injury, stroke, amyotrophic lateral sclerosis, and multiple sclerosis, is also addressed. Therefore, this review gathers the most relevant findings related to the APOE genotype up to date and its implications on AD and CNS pathologies to provide a deeper understanding of the knowledge in the APOE field.

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Section: Implications Of Apoe In Other Neurodegene...mentioning

confidence: 99%

APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer’s disease pathology and brain diseases

Fernández-Calle

Konings

Frontiñán-Rubio

et al. 2022

Mol Neurodegeneration

114

View full text Add to dashboard Cite

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“…This TBI model is of particular relevance to our AD study as an increased risk of dementia in individuals with a TBI diagnosis has been reported in numerous but not all epidemiological evaluations. 48 , 49 , 50 Finally, behavioral impairments in 5xFAD mice were validated in a separate cohort of mice in Figure S4 .…”

Section: New or Updated Hypothesismentioning

confidence: 99%

Role of chronic neuroinflammation in neuroplasticity and cognitive function: A hypothesis

Lecca

Jung

Scerba

et al. 2022

Alzheimer's & Dementia

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Objective Evaluating the efficacy of 3,6’‐dithioPomalidomide in 5xFAD Alzheimer's disease (AD) mice to test the hypothesis that neuroinflammation is directly involved in the development of synaptic/neuronal loss and cognitive decline. Background Amyloid‐β (Aβ) or tau‐focused clinical trials have proved unsuccessful in mitigating AD‐associated cognitive impairment. Identification of new drug targets is needed. Neuroinflammation is a therapeutic target in neurodegenerative disorders, and TNF‐α a pivotal neuroinflammatory driver. New hypothesis AD‐associated chronic neuroinflammation directly drives progressive synaptic/neuronal loss and cognitive decline. Pharmacologically mitigating microglial/astrocyte activation without altering Aβ generation will define the role of neuroinflammation in AD progression. Major challenges Difficulty of TNF‐α‐lowering compounds reaching brain, and identification of a therapeutic‐time window to preserve the beneficial role of neuroinflammatory processes. Linkage to other major theories Microglia/astroglia are heavily implicated in maintenance of synaptic plasticity/function in healthy brain and are disrupted by Aβ. Mitigation of chronic gliosis can restore synaptic homeostasis/cognitive function.

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“…Several investigations of remote mTBI within aging studies showed no significant effect on the likelihood of developing dementia (Dams-O'Connor et al 2013;Grasset et al 2020) or cortical Aβ burden (Crane et al 2016;Sugarman et al 2019a, b;Wang et al 2017;Weiner et al 2017) among cognitively normal adults. Others suggested an association of remote Joel H. Kramer and Raquel C. Gardner equally contributing senior authors.…”

Section: Introductionmentioning

confidence: 99%

Association of remote mild traumatic brain injury with cortical amyloid burden in clinically normal older adults

Asken

Mantyh

Joie

et al. 2021

Brain Imaging and Behavior

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We investigated whether clinically normal older adults with remote, mild traumatic brain injury (mTBI) show evidence of higher cortical Aβ burden. Our study included 134 clinically normal older adults (age 74.1 ± 6.8 years, 59.7% female, 85.8% white) who underwent Aβ positron emission tomography (Aβ-PET) and who completed the Ohio State University Traumatic Brain Injury Identification questionnaire. We limited participants to those reporting injuries classified as mTBI. A subset (N = 30) underwent a second Aβ-PET scan (mean 2.7 years later). We examined the effect of remote mTBI on Aβ-PET burden, interactions between remote mTBI and age, sex, and APOE status, longitudinal Aβ accumulation, and the interaction between remote mTBI and Aβ burden on memory and executive functioning. Of 134 participants, 48 (36%) reported remote mTBI (0, N = 86; 1, N = 31, 2+, N = 17; mean 37 ± 23 years since last mTBI). Effect size estimates were small to negligible for the association of remote mTBI with Aβ burden (p = .94, η 2 < 0.01), and for all interaction analyses. Longitudinally, we found a non-statistically significant association of those with remote mTBI (N = 11) having a faster rate of Aβ accumulation (B = 0.01, p = .08) than those without (N = 19). There was no significant interaction between remote mTBI and Aβ burden on cognition. In clinically normal older adults, history of mTBI is not associated with greater cortical Aβ burden and does not interact with Aβ burden to impact cognition. Longitudinal analyses suggest remote mTBI may be associated with more rapid cortical Aβ accumulation. This finding warrants further study in larger and more diverse samples with well-characterized lifelong head trauma exposure.

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Association of traumatic brain injury with dementia and memory decline in older adults in the United States

Cited by 30 publications

References 46 publications

APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer’s disease pathology and brain diseases

APOE in the bullseye of neurodegenerative diseases: impact of the APOE genotype in Alzheimer’s disease pathology and brain diseases

Role of chronic neuroinflammation in neuroplasticity and cognitive function: A hypothesis

Association of remote mild traumatic brain injury with cortical amyloid burden in clinically normal older adults

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