Head injury as a risk factor for Alzheimer's disease

Mortimer, James A.; French, L. R.; Hutton, J. Thomas; Schuman, Leonard M.

doi:10.1212/wnl.35.2.264

Cited by 269 publications

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“…We discuss the factors that influence the strength and direction of the relationship between TBI and Alzheimer's disease, and the implications of this body of research for patient care and future research. is associated with increased risk for degenerative neurocognitive conditions resulting in dementia [11][12][13][14][15]. AD is by far the most commonly diagnosed subtype of dementia, accounting for up to 80% of all dementia cases [16].…”

Section: Future Perspective: Implications For Patient Carementioning

confidence: 99%

Traumatic Brain Injury As a Risk Factor for Alzheimer’s Disease: Current Knowledge and Future Directions

Dams-O’Connor

Guetta

Hahn-Ketter

et al. 2016

Neurodegener. Dis. Manag.

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There is growing concern about the late effects of traumatic brain injury (TBI). This scoping review summarizes clinical research from the past 10 years that evaluates the relationship between TBI and Alzheimer's disease. This review identified five studies that found increased risk for dementia after TBI, two studies that found no increased risk and four studies that found a relationship only under certain conditions or in specified subsamples. Methodological differences across studies preclude direct comparison of results, and discrepant findings elucidate the complex course of post-TBI neurodegeneration. We discuss the factors that influence the strength and direction of the relationship between TBI and Alzheimer's disease, and the implications of this body of research for patient care and future research.

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Section: Future Perspective: Implications For Patient Carementioning

confidence: 99%

Traumatic Brain Injury As a Risk Factor for Alzheimer’s Disease: Current Knowledge and Future Directions

Dams-O’Connor

Guetta

Hahn-Ketter

et al. 2016

Neurodegener. Dis. Manag.

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“…Risk factors for development of dementia in population studies of elderly normal subjects may be of prognostic value in patients with mild cognitive impairment. The risk factors that derive from the literature include age, 29,30 a family history of dementia, 31 history of head injury, 32,33 depression, 34,35 as well as low pre-morbid intelligence and education. [36][37][38] Female gender has been noted to be a risk factor for dementia in a number of studies, 30,[39][40][41] although this has not been found in others.…”

Section: Clinical Risk Factors For Development Of Dementia and Admentioning

confidence: 99%

Can Clinical Data Predict Progression to Dementia in Amnestic Mild Cognitive Impairment?

Fellows

Bergman²,

Wolfson³

et al. 2008

Can. j. neurol. sci.

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314As treatments to alleviate symptoms and to slow the progression of Alzheimer's disease (AD) emerge, an increasingly urgent dilemma for physicians is also developing: which of the many elderly individuals with memory complaints will develop Alzheimer's disease, and would therefore be candidates for preventive therapies? An important goal of current research must be to establish useful pre-clinical diagnostic and predictive guidelines, and this can only emerge from longitudinal follow-up of elderly individuals with mild memory loss. In this paper, we report the clinical characteristics of such a group, with the aim of ABSTRACT: Background: To determine whether clinical data obtained by history and physical examination can predict eventual progression to dementia in a cohort of elderly people with mild cognitive impairment. Methods: A prospective, longitudinal study of a cohort of elderly subjects with amnestic Mild Cognitive Impairment (MCI). Ninety subjects meeting the criteria for amnestic MCI were recruited and followed annually for an average of 3.3 years. Main outcome measure was the development of dementia determined by clinical assessment with confirmatory neuropsychological evaluation. Results: Fifty patients (56%) developed dementia on follow-up. They were older, had lower Mini-mental status exam (MMSE) scores and a shorter duration of symptoms at the time of first assessment. Multivariate logistic regression analysis identified age at symptom onset as the only clinical parameter which distinguished the group that deteriorated to dementia from the group that did not. The odds ratio for age was 1.1 (confidence interval 1.04 -1.18). Conclusions: Patients presenting with amnestic MCI insufficient for the diagnosis of dementia are at high risk of developing dementia on follow-up. In our cohort, 56% were diagnosed with dementia over an average period of 5.9 years from symptom onset. The only clinical predictor for the eventual development of dementia was older age at symptom onset. Clinical features alone were insufficient to predict development of dementia.RÉSUMÉ: Les données cliniques peuvent-elles prédire la progression vers la démence dans l'atteinte cognitive légère avec syndrome amnésique? Contexte : Le but de cette étude était de déterminer si les données cliniques provenant de l'histoire médicale et de l'examen physique peuvent prédire la progression éventuelle vers la démence dans une cohorte de gens âgés ayant une atteinte cognitive légère. Méthodes : Il s'agit d'une étude longitudinale prospective d'une cohorte de sujets âgés ayant une atteinte cognitive légère (ACL). Quatre-vingt-dix sujets rencontrant les critères diagnostiques de l'ACL amnésique ont été recrutés et suivis annuellement pendant 3,3 ans en moyenne. Le critère d'évaluation principal était l'apparition d'une démence selon l'évaluation clinique confirmée par une évaluation neuropsychologique. Résultats : Cinquante patients (56%) ont développé une démence au cours du suivi. Ils étaient plus âgés, avaient des scores MMSE plus bas et u...

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“…The interest in the role of Ab after TBI has grown from epidemiological studies that have demonstrated an association between a history of TBI and the development of AD later in life (Graves et al, 1990;Mortimer et al, 1985Mortimer et al, , 1991Salib and Hillier, 1997;Szczygielski et al, 2005;Van Den Heuvel et al, 2007). Additionally, post-mortem studies have demonstrated AD-like deposits of Ab in as many as 30% of TBI victims (Roberts et al, 1991(Roberts et al, , 1994.…”

Section: Introductionmentioning

confidence: 99%

Detrimental Effect of Genetic Inhibition of B-Site App-Cleaving Enzyme 1 on Functional Outcome after Controlled Cortical Impact in Young Adult Mice

Mannix

Zhang

Park

et al. 2011

Journal of Neurotrauma

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Abstractb-Amyloid (Ab) peptides, most notably associated with Alzheimer's disease, have been implicated in the pathogenesis of secondary injury after traumatic brain injury (TBI). A prior study has demonstrated that blocking the b-site amyloid precursor protein (APP)-cleaving enzyme 1 (Bace1) required for production of Ab from APP improved functional and histologic outcomes after controlled cortical impact (CCI) in aged mice. However, the majority of patients with severe TBI are young adults under the age of 40. Prior experimental models have suggested age-dependent differences in Ab clearance, and a recent study in our lab suggests that young animals remediate acute elevations in Ab after CCI better than older animals. We therefore tested the hypothesis that Bace1 deletion in young adult mice would not be protective after CCI. Male Bace1 knockout (Bace1 -/-) and wild-type Bace1 +/+ (C57BL/6) mice (2-3 months old) were subjected to CCI (n = 18-23/group) or sham injury (n = 10-12/group). Functional outcomes were assessed with wire grip (motor) and the Morris water maze (MWM; spatial memory). Soluble Ab levels were assessed at 48 h after CCI. Histopathological outcomes were assessed by lesion and hippocampal volume. Clustered ordinal logistic regression showed overall significant impairment in motor performance in injured Bace1-/-versus Bace1 +/+ animals ( p = 0.003). No significant differences in MWM performance were found on repeated-measures ANOVA ( p = 0.11) between groups. Probe scores were significantly worse in injured Bace1-/-versus Bace1 +/+ mice ( p = 0.0009). Soluble Ab 40 was significantly lower in ipsilateral hemispheres of Bace1 -/-than in Bace1 +/+ animals after CCI (0.9 [IQR 0.88-0.94] pmol/g protein versus 3.8 [IQR 2.4-6.0] pmol/g protein; p = 0.005). Lesion and hippocampal volumes did not differ between injured groups. The data suggest that therapies targeting Bace1 may need to be tailored according to age and injury severity, as their use may exacerbate functional deficits after TBI in younger or less severely injured patients.

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Head injury as a risk factor for Alzheimer's disease

Cited by 269 publications

References 0 publications

Traumatic Brain Injury As a Risk Factor for Alzheimer’s Disease: Current Knowledge and Future Directions

Traumatic Brain Injury As a Risk Factor for Alzheimer’s Disease: Current Knowledge and Future Directions

Can Clinical Data Predict Progression to Dementia in Amnestic Mild Cognitive Impairment?

Detrimental Effect of Genetic Inhibition of B-Site App-Cleaving Enzyme 1 on Functional Outcome after Controlled Cortical Impact in Young Adult Mice

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