scholarly journals Reaction Time Decomposition as a Tool to Study Subcortical Ischemic Vascular Cognitive Impairment

2021 ◽  
pp. 1-11
Author(s):  
Emma Richards ◽  
Andrea Tales ◽  
Antony Bayer ◽  
Jade E. Norris ◽  
Claire Hanley ◽  
...  

Background: The study of reaction time (RT) and its intraindividual variability (IIV) in aging, cognitive impairment, and dementia typically fails to investigate the processing stages that contribute to an overall response. Applying “mental chronometry” techniques makes it possible to separately assess the role of processing components during environmental interaction. Objective: To determine whether RT and IIV-decomposition techniques can shed light on the nature of underlying deficits in subcortical ischemic vascular cognitive impairment (VCI). Using a novel iPad task, we examined whether VCI deficits occur during both initiation and movement phases of a response, and whether they are equally reflected in both RT and IIV. Methods: Touch cancellation RT and its IIV were measured in a group of younger adults (n = 22), cognitively healthy older adults (n = 21), and patients with VCI (n = 21) using an iPad task. Results: Whereas cognitively healthy aging affected the speed (RT) of response initiation and movement but not its variability (IIV), VCI resulted in both slowed RT and increased IIV for both response phases. Furthermore, there were group differences with respect to response phase. Conclusion: These results indicate that IIV can be more sensitive than absolute RT in separating VCI from normal aging. Furthermore, compared to cognitively healthy aging, VCI was characterized by significant deficits in planning/initiating action as well as performing movements. Such deficits have important implications for real life actions such as driving safety, employment, and falls risk.

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 622-623
Author(s):  
Burcu Demiray ◽  
Minxia Luo ◽  
Mike Martin

Abstract Using smartphone sensing in real life, we examined conversational time travel (i.e., talking about the personal past versus future), its functions and relation with positive affect (i.e., laughing behavior). We used the Electronically Activated Recorder (audio recorder that periodically records snippets of ambient sounds and speech) and collected a random sample of over 30,000 sound snippets (30 seconds long) from 61 young and 48 healthy older adults across four days. We transcribed and manually coded participants’ speech. Multilevel models conducted in R showed that individuals tended to talk about their past with more social functions (e.g., give advice), whereas talked about their future for more directive purposes (e.g., planning). Age group differences were minimal. We also found that individuals laughed two times more while talking about their past than their future. Results are discussed in relation to the functions of mental/conversational time travel in the context of healthy aging.


2019 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  

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.


2019 ◽  
Vol 25 (3) ◽  
pp. 249-265
Author(s):  
Paul T. Cirino ◽  
Paulina A. Kulesz ◽  
Amanda E. Child ◽  
Ashley L. Ware ◽  
Marcia A. Barnes ◽  
...  

AbstractObjectives: Fluency is a major problem for individuals with neurodevelopmental disorders, including fluency deficits for academic skills. The aim of this study was to determine neurocognitive predictors of academic fluency within and across domains of reading, writing, and math, in children and adults, with and without spina bifida. In addition to group differences, we expected some neurocognitive predictors (reaction time, inattention) to have similar effects for each academic fluency outcome, and others (dexterity, vocabulary, nonverbal reasoning) to have differential effects across outcomes. Methods: Neurocognitive predictors were reaction time, inattention, dexterity, vocabulary, and nonverbal reasoning; other factors included group (individuals with spina bifida, n=180; and without, n=81), age, and demographic and untimed academic content skill covariates. Univariate and multivariate regressions evaluated hypotheses. Results: Univariate regressions were significant and robust (R2=.78, .70, .73, for reading, writing, and math fluency, respectively), with consistent effects of covariates, age, reaction time, and vocabulary; group and group moderation showed small effect sizes (<2%). Multivariate contrasts showed differential prediction across academic fluency outcomes for reaction time and vocabulary. Conclusions: The novelty of the present work is determining neurocognitive predictors for an important outcome (academic fluency), within and across fluency domains, across population (spina bifida versus typical), over a large developmental span, in the context of well-known covariates. Results offer insight into similarities and differences regarding prediction of different domains of academic fluency, with implications for addressing academic weakness in spina bifida, and for evaluating similar questions in other neurodevelopmental disorders. (JINS, 2019, 25, 249–265)


2020 ◽  
Vol 21 (6) ◽  
pp. 2176 ◽  
Author(s):  
Amelia Nur Vidyanti ◽  
Jia-Yu Hsieh ◽  
Kun-Ju Lin ◽  
Yao-Ching Fang ◽  
Ismail Setyopranoto ◽  
...  

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.


2019 ◽  
Vol 72 (3) ◽  
pp. 845-857 ◽  
Author(s):  
Emma Richards ◽  
Antony Bayer ◽  
Jeremy J. Tree ◽  
Claire Hanley ◽  
Jade E. Norris ◽  
...  

2020 ◽  
Vol 10 (12) ◽  
pp. 919
Author(s):  
Giuseppe Forte ◽  
Maria Casagrande

Introduction: Cognitive functions play a crucial role in daily functioning. Unfortunately, some cognitive abilities decline in the process of healthy aging. An increasing body of evidence has highlighted the role of lifestyle habits and cardiovascular diseases, such as high blood pressure, in increasing the risk of cognitive decline. Surprisingly, although hypertension is a modifiable risk factor for cerebrovascular damage, the role of hypertension on cognitive impairment development is not still clear. Several key questions remain unresolved, and there are many inconsistent results in studies considering this topic. This review is aimed to systematically analyze the results found by the studies that investigated whether high blood pressure, in both hypertensive and healthy people, is related to cognitive performance. Furthermore, it points to evaluate the role of age in this relationship. Method: The review process was conducted according to the PRISMA statement. Restrictions were made, selecting the studies in English and published in peer-review journals, including at least one cognitive measure and blood pressure measurement. Studies that included participants with medical conditions, dementia, psychiatric disorders, strokes, and brain injury were excluded. Cross-sectional and longitudinal studies were analyzed separately. Finally, blood pressure measured at young life (18–39 years), midlife (age 40–64 years), elderly (65–74 years), and old age (≥75 years) were considered. Results: The review allows 68 studies to be selected, which include 154,935 participants. The results provided evidence of an adverse effect of exposure to high blood pressure on cognitive performance. High blood pressure in midlife was linked with poorer cognitive functioning; this evidence was found in cross-sectional and longitudinal studies. However, this association declines with increasing age and tends to become inconsistent. In older people, the relationship between blood pressure and cognitive performance is non-linear, highlighting a beneficial effect of high blood pressure on cognition. Conclusions: Despite some limitations, this review showed that cardiovascular and neuro-cognitive systems do not operate in isolation, but they are related. Blood pressure can be considered an early biomarker of cognitive impairment, and the necessity of early blood pressure measurement and control was underlined.


2017 ◽  
Vol 144 (5) ◽  
pp. 582-594 ◽  
Author(s):  
Elizabeth Dao ◽  
Ging-Yuek Robin Hsiung ◽  
Teresa Liu-Ambrose

2020 ◽  
Vol 12 (5) ◽  
pp. 84-91
Author(s):  
A. G. Gogoleva ◽  
V. V. Zakharov

The paper presents the current etiopathogenetic classification of chronic cerebrovascular diseases (CVD) and discusses the role of hypertension, cerebral amyloid angiopathy, and genetically determined syndromes in the development of this pathological condition. It gives recommendations for the neuroradiological diagnosis of chronic CVD in accordance with the international standards. The paper discusses the clinical manifestations of chronic CVD, primarily vascular cognitive impairment. It discusses international guidelines for the examination and treatment of patients with chronic CVD, as well as the rules for stroke prevention in this patient cohort. The possibilities of pathogenetically based therapy in decreasing the severity of vascular cognitive impairment in the presence of chronic CVD are also highlighted.


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