scholarly journals Neuroimaging and Psychometric Assessment of Mild Cognitive Impairment After Traumatic Brain Injury

2020 ◽  
Vol 11 ◽  
Author(s):  
Maria Calvillo ◽  
Andrei Irimia
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Psychometric Assessment

scholarly journals Traumatic brain injury history and progression from mild cognitive impairment to Alzheimer disease.

2018 ◽  
Vol 32 (4) ◽  
pp. 401-409 ◽  
Author(s):  
Christian LoBue ◽  
Fu L. Woon ◽  
Heidi C. Rossetti ◽  
Linda S. Hynan ◽  
John Hart ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Alzheimer Disease

scholarly journals Self-Reported Traumatic Brain Injury and Mild Cognitive Impairment: Increased Risk and Earlier Age of Diagnosis

2016 ◽  
Vol 51 (3) ◽  
pp. 727-736 ◽  
Author(s):  
Christian LoBue ◽  
David Denney ◽  
Linda S. Hynan ◽  
Heidi C. Rossetti ◽  
Laura H. Lacritz ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Increased Risk ◽  
Age Of Diagnosis

P1-238: Traumatic brain injury history and age of mild cognitive impairment diagnosis

2015 ◽  
Vol 11 (7S_Part_9) ◽  
pp. P444-P444
Author(s):  
Munro Cullum ◽  
Christian Lobue ◽  
David Denney ◽  
Linda Hynan ◽  
Heidi Rossetti ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury

scholarly journals Mild cognitive impairment and structural brain abnormalities in a sexagenarian with a history of childhood traumatic brain injury

2017 ◽  
Vol 96 (4) ◽  
pp. 652-660 ◽  
Author(s):  
John Darrell Van Horn ◽  
Andrei Irimia ◽  
Carinna M. Torgerson ◽  
Avnish Bhattrai ◽  
Zachary Jacokes ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Brain Abnormalities ◽  
History Of Childhood ◽  
History Of ◽  
Structural Brain

scholarly journals The Effect of Traumatic Brain Injury on Alzheimer’s Disease and Cognitive Decline in Veterans and Non-Veterans

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 305-306
Author(s):  
Igor Akushevich ◽  
Arseniy Yashkin ◽  
Stanislav Kolpakov Nikitin ◽  
Julia Kravchenko
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Cognitive Decline ◽  
Cognitive Status ◽  
Risk Scores ◽  
Post Traumatic Stress

Abstract We assess the differences in the effect of traumatic brain injury (TBI) on the decline in cognitive status and the risk of Alzheimer’s disease and related dementia (AD/ADRD) between veteran and non-veteran respondents of the Health and Retirement Study (HRS) and measure the sensitivity of these differences to the incremental introduction of controls for associated risk factors. Three groups of AD/ADRD risk-related variables were used: i) demographic/socioeconomic factors, including gender, race, marital status, education, income, and the number of limitations in activities of daily living; ii) comorbidities, including co-existing depression/post-traumatic stress syndrome (PTSD), substance (alcohol, tobacco and/or prescription drug) abuse, diabetes mellitus, stroke, and heart failure; and iii) genetic factors, including the presence of at least one pair of the APOE4 allele and a series of polygenic risk scores associated with AD hallmarks. The dynamics of changes in cognitive impairment in response to TBI, PTSD, and mild cognitive impairment were validated against respective measures estimated using the Department of Defense Alzheimer’s Disease Neuroimaging Initiative (DoD-ADNI) data. The results of the analyses showed that TBI and PTSD were strongly associated with cognitive decline and the risks of AD/ADRD in both veteran and non-veteran subpopulations in HRS data and the difference between them was not statistically significant. Effect magnitude decreased with the addition of risk-related control variables but remained associated with the increased risks. Prevalence of mild cognitive impairment was associated with TBI at baseline in DoD-ADNI data, but no cognitive decline was observed during one year of follow-up.

scholarly journals Evaluating the Memory Enhancing Effects of Angelica gigas in Mouse Models of Mild Cognitive Impairments

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 97
Author(s):  
Minsang Kim ◽  
Minah Song ◽  
Hee-Jin Oh ◽  
Jin Hui ◽  
Woori Bae ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Spatial Learning ◽  
Chronic Mild Stress ◽  
Fear Memory ◽  
Mild Stress ◽  
Angelica Gigas

(1) Background: By 2050, it is estimated that 130 million people will be diagnosed with dementia, and currently approved medicines only slow the progression. So preventive intervention is important to treat dementia. Mild cognitive impairment is a condition characterized by some deterioration in cognitive function and increased risk of progressing to dementia. Therefore, the treatment of mild cognitive impairment (MCI) is a possible way to prevent dementia. Angelica gigas reduces neuroinflammation, improves circulation, and inhibits cholinesterase, which can be effective in the prevention of Alzheimer’s disease and vascular dementia and the progression of mild cognitive impairment. (2) Methods: Angelica gigas (AG) extract 1 mg/kg was administered to mildly cognitive impaired mice, models based on mild traumatic brain injury and chronic mild stress. Then, spatial, working, and object recognition and fear memory were measured. (3) Result: Angelica gigas improved spatial learning, working memory, and suppressed fear memory in the mild traumatic brain injury model. It also improved spatial learning and suppressed cued fear memory in the chronic mild stress model animals. (4) Conclusions: Angelica gigas can improve cognitive symptoms in mild cognitive impairment model mice.

scholarly journals Mild Cognitive Impairment in Chronic Brain Injury Associated with Serum Anti-AP3B2 Autoantibodies: Report and Literature Review

2021 ◽  
Vol 11 (9) ◽  
pp. 1208
Author(s):  
Niels Hansen ◽  
Claudia Bartels ◽  
Jens Wiltfang ◽  
Winfried Stöcker ◽  
Dirk Fitzner
Keyword(s):  
Traumatic Brain Injury ◽  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Brain Injury ◽  
Brain Damage ◽  
Adaptor Protein ◽  
Gait Disturbance ◽  
Disease Case ◽  
The Right ◽  
The Brain

Background: Chronic traumatic brain injury is a condition that predisposes the brain to activate B-cells and produce neural autoantibodies. Anti-adaptor protein 3, subunit B2 (AP3B2) autoantibodies have thus far been associated with diseases affecting the cerebellum or vestibulocerebellum. Through this case report, we aim to broaden the spectrum of anti-AP3B2-associated disease. Case description: We report on a 51-year-old woman with a brain injury approximately 28 years ago who recently underwent neuropsychological testing, magnetic resonance imaging of the brain (cMRI), and cerebrospinal fluid (CSF) analysis. Neural autoantibodies were determined in serum and CSF. Our patient suffered from mild cognitive impairment (amnestic MCI, multiple domains) with stable memory deficits and a decline in verbal fluency and processing speed within a two-year interval after the first presentation in our memory clinic. Brain MRI showed brain damage in the right temporoparietal, frontolateral region and thalamus, as well as in the left posterior border of the capsula interna and white matter in the frontal region. Since the brain damage, she suffered paresis of the upper extremities on the left side and lower extremities on the right side as well as gait disturbance. Our search for autoantibodies revealed anti-AP3B2 autoantibodies in serum. Conclusions: Our report expands the spectrum of symptoms to mild cognitive impairment in addition to a gait disturbance associated with anti-AP3B2 autoantibodies. Furthermore, it is conceivable that a prior traumatic brain injury could initiate the development of anti-AP3B2-antibody-associated brain autoimmunity, reported here for the first time.

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