scholarly journals Explanatory role of sociodemographic, clinical, behavioral, and social factors on cognitive decline in older adults with diabetes

2022 ◽  
Vol 22 (1) ◽  
Author(s):  
Sean M. O’Toole ◽  
Rebekah J. Walker ◽  
Emma Garacci ◽  
Aprill Z. Dawson ◽  
Jennifer A. Campbell ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Social Factors ◽  
Ethnic Disparities ◽  
Personal Control ◽  
Estimating Equation ◽  
Explanatory Role ◽  
Racial Ethnic ◽  
Normal Cognition

Abstract Background The aim of the study was to examine the explanatory role of sociodemographic, clinical, behavioral, and social factors on racial/ethnic differences in cognitive decline among adults with diabetes. Methods Adults aged 50+ years with diabetes from the Health and Retirement Survey were assessed for cognitive function (normal, mild cognitive impairment [MCI], and dementia). Generalized estimating equation (GEE) logistic regression models were used to account for repeating measures over time. Models were adjusted for sociodemographic (gender, age, education, household income and assets), behavioral (smoking), clinical (ie. comorbidities, body mass index), and social (social support, loneliness, social participation, perceived constraints and perceived mastery on personal control) factors. Results Unadjusted models showed non-Hispanic Blacks (NHB) and Hispanics were significantly more likely to progress from normal cognition to dementia (NHB OR: 2.99, 95%CI 2.35–3.81; Hispanic OR: 3.55, 95%CI 2.77–4.56), and normal cognition to MCI (NHB OR = 2.45, 95%CI 2.14–2.82; Hispanic OR = 2.49, 95%CI 2.13–2.90) compared to non-Hispanic Whites (NHW). Unadjusted models for the transition from mild cognitive decline to dementia showed Hispanics were more likely than NHW to progress (OR = 1.43, 95%CI 1.11–1.84). After adjusting for sociodemographic, clinical/behavioral, and social measures, NHB were 3.75 times more likely (95%CI 2.52–5.56) than NHW to reach dementia from normal cognition. NHB were 2.87 times more likely (95%CI 2.37–3.48) than NHW to reach MCI from normal. Hispanics were 1.72 times more likely (95%CI 1.17–2.52) than NHW to reach dementia from MCI. Conclusion Clinical/behavioral and social factors did not explain racial/ethnic disparities. Racial/ethnic disparities are less evident from MCI to dementia, emphasizing preventative measures/interventions before cognitive impairment onset are important.

scholarly journals The Role of High Triglycerides Level in Predicting Cognitive Impairment: A Review of Current Evidence

Nutrients ◽  
2021 ◽  
Vol 13 (6) ◽  
pp. 2118
Author(s):  
Alina Mihaela Dimache ◽  
Delia Lidia Șalaru ◽  
Radu Sascău ◽  
Cristian Stătescu
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Lifestyle Modification ◽  
Cognitive Disorders ◽  
Current Evidence ◽  
Barrier Dysfunction ◽  
Serum Triglycerides ◽  
Cerebral Amyloidosis ◽  
The Relationship

The burden of cognitive disorders is huge and still growing, however the etiology and the degree of cognitive impairment vary considerably. Neurodegenerative and vascular mechanisms were most frequently assessed in patients with dementia. Recent studies have shown the possible involvement of triglycerides levels in cognitive function through putative mechanisms such as brain blood barrier dysfunction or amyloid metabolism imbalance, but not all research in the field found this association. Several clinical studies evaluated the relationship between different forms of cognitive decline and levels of serum triglycerides, independent of other cardiovascular risk factors. This review focuses on the role of triglycerides in cognitive decline, cerebral amyloidosis and vascular impairment. Considering that the management of hypertriglyceridemia benefits from lifestyle modification, diet, and specific drug therapy, future studies are requested to appraise the triglycerides–cognitive impairment relationship.

Psychotherapy racial/ethnic disparities in treatment outcomes: The role of university racial/ethnic composition.

2021 ◽  
Author(s):  
Jesse Owen ◽  
Jeremy Coleman ◽  
Joanna M. Drinane ◽  
Karen Tao ◽  
Zac Imel ◽  
...  
Keyword(s):  
Treatment Outcomes ◽  
Ethnic Disparities ◽  
Ethnic Composition ◽  
Racial Ethnic

scholarly journals Racial/Ethnic Disparities in Failure to Initiate HIV Care: Role of HIV Testing Site, Individual Factors, and Neighborhood Factors, Florida, 2014–2015

2018 ◽  
Vol 29 (3) ◽  
pp. 1153-1175
Author(s):  
Mary Jo Trepka ◽  
Diana M. Sheehan ◽  
Kristopher P. Fennie ◽  
Daniel E. Mauck ◽  
Spencer Lieb ◽  
...  
Keyword(s):  
Hiv Testing ◽  
Ethnic Disparities ◽  
Hiv Care ◽  
Individual Factors ◽  
Neighborhood Factors ◽  
Testing Site ◽  
Racial Ethnic

scholarly journals Risk of progression from subjective cognitive decline to mild cognitive impairment: The role of study setting

2018 ◽  
Vol 14 (6) ◽  
pp. 734-742 ◽  
Author(s):  
Beth E. Snitz ◽  
Tianxiu Wang ◽  
Yona Keich Cloonan ◽  
Erin Jacobsen ◽  
Chung-Chou H. Chang ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Mild Cognitive Impairment ◽  
Cognitive Decline ◽  
Subjective Cognitive Decline ◽  
Risk Of Progression ◽  
Study Setting

School Punishment and Education: Racial/Ethnic Disparities With Grade Retention and the Role of Urbanicity

2018 ◽  
pp. 004208591880143 ◽  
Author(s):  
Anthony A. Peguero ◽  
Kay S. Varela ◽  
Miner P. “Trey” Marchbanks ◽  
Jamilia Blake ◽  
John M. Eason
Keyword(s):  
Grade Retention ◽  
Ethnic Disparities ◽  
School Punishment ◽  
Racial Ethnic

The role of high-mobility group box protein 1 in chronic cerebral hypoperfusion-induced vascular cognitive impairment animals

2019 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  
Keyword(s):  
Cognitive Impairment ◽  
Cognitive Decline ◽  
High Mobility ◽  
Vascular Cognitive Impairment ◽  
High Mobility Group ◽  
Cerebral Hypoperfusion ◽  
Hippocampal Atrophy ◽  
Amyloid Pet ◽  
Knock Out

Abstract Background: The molecular mechanisms of vascular cognitive impairment (VCI) are diverse and still in puzzle. VCI could be attributed to chronic cerebral hypoperfusion (CCH). CCH may cause a cascade of reactions involved in ischemia and neuro-inflammation which plays important roles in the pathophysiology of VCI. High-mobility group box protein 1 (HMGB1) is a non-histone protein that serves as a damage-associated molecular signal leading to cascades of inflammation. Increased level of HMGB1 has been established in the acute phase of CCH. However, the role of HMGB1 at the chronic phase of CCH remains elucidated. Methods: We performed modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice to induce CCH. We examined the cerebral blood flow (CBF) reduction by laser doppler flowmetry, the protein expression of HMGB1 and its pro-inflammatory cytokines (TNF-a, IL-1b, and IL-6) by western blotting and immunohistochemistry. The brain pathology was assessed by 7T-animal MRI and amyloid-b accumulation was assessed by amyloid-PET scanning. We further evaluated the effect of HMGB1 suppression by injecting CRISPR/Cas9 knock-out plasmid intra-hippocampus bilaterally. Results: There were reduction of CBF up to 50% which persisted three months after CCH. The modified-BCCAO animals developed significant cognitive decline. The 7T-MRI image showed hippocampal atrophy, although the amyloid-PET showed no significant amyloid-beta accumulation. Increased protein levels of HMGB1, TNF-a and IL-1b were found three months after BCCAO. HMGB1 suppression by CRISPR/Cas9 knock-out plasmid restored the CBF, IL-1B, TNF-alpha, IL-6, and attenuated hippocampal atrophy and cognitive decline. Conclusion: HMGB1 plays a pivotal role in the pathophysiology of the animal model of CCH and it might be a candidate as therapeutic targets of VCI.

scholarly journals Sleep Disturbance and the Risk of Cognitive Decline or Clinical Conversion in the ADNI Cohort

2018 ◽  
Vol 45 (3-4) ◽  
pp. 232-242 ◽  
Author(s):  
Adam P. Mecca ◽  
Hannah R. Michalak ◽  
Julia W. McDonald ◽  
Emily C. Kemp ◽  
Erika A. Pugh ◽  
...  
Keyword(s):  
Cohort Study ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Sleep Disturbance ◽  
Secondary Analysis ◽  
Study Results ◽  
Global Cognition ◽  
The Relationship ◽  
Normal Cognition

Background: We investigated the relationship between sleep disturbance and cognitive decline or clinical conversion in individuals with normal cognition (CN), as well as those with mild cognitive impairment (MCI) and dementia due to Alzheimer disease (AD-dementia). Methods: Secondary analysis of 1,629 adults between 48 and 91 years of age with up to 24 months of follow-up from the ADNI (Alzheimer’s Disease Neuroimaging Initiative), a longitudinal cohort study. Results: Sleep disturbance was not associated with decline in memory, executive function, or global cognition. The presence of sleep disturbance did not significantly increase the risk of diagnostic conversion in CN, early MCI, or late MCI participants. Conclusion: This study investigated the effect of sleep disturbance on cognitive decline using several outcomes and does not support the hypothesis that sleep disturbance predicts subsequent cognitive decline.

scholarly journals Role of HMGB1 in an Animal Model of Vascular Cognitive Impairment Induced by Chronic Cerebral Hypoperfusion

2020 ◽  
Vol 21 (6) ◽  
pp. 2176 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  
Keyword(s):  
Animal Model ◽  
Cognitive Impairment ◽  
Cognitive Decline ◽  
Chronic Phase ◽  
Vascular Cognitive Impairment ◽  
Chronic Cerebral Hypoperfusion ◽  
Cerebral Hypoperfusion ◽  
Hippocampal Atrophy ◽  
Tnf Α

The pathophysiology of vascular cognitive impairment (VCI) is associated with chronic cerebral hypoperfusion (CCH). Increased high-mobility group box protein 1 (HMGB1), a nonhistone protein involved in injury and inflammation, has been established in the acute phase of CCH. However, the role of HMGB1 in the chronic phase of CCH remains unclear. We developed a novel animal model of CCH with a modified bilateral common carotid artery occlusion (BCCAO) in C57BL/6 mice. Cerebral blood flow (CBF) reduction, the expression of HMGB1 and its proinflammatory cytokines (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-1β, and IL-6), and brain pathology were assessed. Furthermore, we evaluated the effect of HMGB1 suppression through bilateral intrahippocampus injection with the CRISPR/Cas9 knockout plasmid. Three months after CCH induction, CBF decreased to 30–50% with significant cognitive decline in BCCAO mice. The 7T-aMRI showed hippocampal atrophy, but amyloid positron imaging tomography showed nonsignificant amyloid-beta accumulation. Increased levels of HMGB1, TNF-α, IL-1β, and IL-6 were observed 3 months after BCCAO. HMGB1 suppression with CRISPR/Cas9 knockout plasmid restored TNF-α, IL-1β, and IL-6 and attenuated hippocampal atrophy and cognitive decline. We believe that HMGB1 plays a pivotal role in CCH-induced VCI pathophysiology and can be a potential therapeutic target of VCI.

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