Cognitive functioning in individuals with Parkinson’s disease and traumatic brain injury: A longitudinal study

Schiehser, Dawn M.; Filoteo, J. Vincent; Litvan, Irene; Pirogovsky‐Turk, Eva; Lessig, Stephanie; Song, David S.

doi:10.1016/j.parkreldis.2016.05.024

Cited by 9 publications

(7 citation statements)

References 11 publications

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“…However, it is important to point out that premanifest individuals presented significantly higher levels of auto-activation deficit than controls. This emphasizes the gradual nature of disease onset, which affects neuropsychiatric functioning years or even decades prior to formal disease diagnosis by motor onset (Ross et al, 2014; Martinez-Horta et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Despite the fact that HD is clinically diagnosed based on motor onset, pathological changes are often present long before motor symptoms (Thompson et al, 2012; Martinez-Horta et al, 2016). As such, when examining the association between white matter microstructure and apathy subtypes, we studied the disease as a continuum.…”

Section: Methodsmentioning

confidence: 99%

“…When studying global apathy via the PBA-s and LARS-s, we utilized the PBA-s ‘affective behavior’ component as a covariate of no interest in order to examine apathy as an independent psychiatric syndrome from depression. (For a similar approach, see Reyes et al (2009), Martinez-Horta et al (2016), and Misiura et al (2019).) Similarly, when studying cognitive apathy, UHDRS-cogscore and TFC effects were also controlled.…”

Section: Methodsmentioning

confidence: 99%

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White matter cortico-striatal tracts predict apathy subtypes in Huntington's disease

Paepe

Sierpowska

García-Gorro

et al. 2019

NeuroImage: Clinical

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Background Apathy is the neuropsychiatric syndrome that correlates most highly with Huntington's disease progression, and, like early patterns of neurodegeneration, is associated with lesions to cortico-striatal connections. However, due to its multidimensional nature and elusive etiology, treatment options are limited. Objectives To disentangle underlying white matter microstructural correlates across the apathy spectrum in Huntington's disease. Methods Forty-six Huntington's disease individuals (premanifest ( N = 22) and manifest ( N = 24)) and 35 healthy controls were scanned at 3-tesla and underwent apathy evaluation using the short-Problem Behavior Assessment and short-Lille Apathy Rating Scale, with the latter being characterized into three apathy domains, namely emotional, cognitive, and auto-activation deficit. Diffusion tensor imaging was used to study whether individual differences in specific cortico-striatal tracts predicted global apathy and its subdomains. Results We elucidate that apathy profiles may develop along differential timelines, with the auto-activation deficit domain manifesting prior to motor onset. Furthermore, diffusion tensor imaging revealed that inter-individual variability in the disruption of discrete cortico-striatal tracts might explain the heterogeneous severity of apathy profiles. Specifically, higher levels of auto-activation deficit symptoms significantly correlated with increased mean diffusivity in the right uncinate fasciculus. Conversely, those with severe cognitive apathy demonstrated increased mean diffusivity in the right frontostriatal tract and left dorsolateral prefrontal cortex to caudate nucleus tract. Conclusions The current study provides evidence that white matter correlates associated with emotional, cognitive, and auto-activation subtypes may elucidate the heterogeneous nature of apathy in Huntington's disease, as such opening a door for individualized pharmacological management of apathy as a multidimensional syndrome in other neurodegenerative disorders.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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White matter cortico-striatal tracts predict apathy subtypes in Huntington's disease

Paepe

Sierpowska

García-Gorro

et al. 2019

NeuroImage: Clinical

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“…Remarkably, full amelioration of the toxic effects of glutamate and hydrogen peroxide were achieved at 1 and 10 nM, respectively, in SH-hGLP-1R#9 cells. In light of the reported dopaminergic neuronal cell loss following mild to moderate TBI in rodent models (Hutson et al, 2011; Bales et al, 2010; Acosta et al, 2015; Impellizzeri et al, 2016), up regulation of PD associated pathways instigated by mTBI in rodents (Tweedie et al, 2013b), elevated risk of PD following TBI in humans (Gardner et al, 2015; Crane et al, 2016), and progression of PD in humans by TBI (Schiehser et al, 2016; Crane et al, 2016), we evaluated the ability of Twincretin to protect cultured dopaminergic primary VM neurons from cellular demise. Twincretin (10 to 1000 nM) significantly increased TH immunoreactivity in these neurons exposed to toxic doses of 6OHDA, as compared to neurons exposed to the toxic insult alone.…”

Section: Discussionmentioning

confidence: 99%

Novel GLP-1R/GIPR co-agonist “twincretin” is neuroprotective in cell and rodent models of mild traumatic brain injury

Tamargo

Bader

et al. 2017

Experimental Neurology

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Several single incretin receptor agonists that are approved for the treatment of type 2 diabetes mellitus (T2DM) have been shown to be neuroprotective in cell and animal models of neurodegeneration. Recently, a synthetic dual incretin receptor agonist, nicknamed “twincretin,” was shown to improve upon the metabolic benefits of single receptor agonists in mouse and monkey models of T2DM. In the current study, the neuroprotective effects of twincretin are probed in cell and mouse models of mild traumatic brain injury (mTBI), a prevalent cause of neurodegeneration in toddlers, teenagers and the elderly. Twincretin is herein shown to have activity at two different receptors, dose-dependently increase levels of intermediates in the neurotrophic CREB pathway and enhance viability of human neuroblastoma cells exposed to toxic concentrations of glutamate and hydrogen peroxide, insults mimicking the inflammatory conditions in the brain post-mTBI. Additionally, twincretin is shown to improve upon the neurotrophic effects of single incretin receptor agonists in these same cells. Finally, a clinically translatable dose of twincretin, when administered post-mTBI, is shown to fully restore the visual and spatial memory deficits induced by mTBI, as evaluated in a mouse model of weight drop close head injury. These results establish twincretin as a novel neuroprotective agent and suggest that it may improve upon the effects of the single incretin receptor agonists via dual agonism.

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“…Conversion to dementia has been predicted by both cognitive features [94,95] as well as a series of non-cognitive features [95][96][97][98][99] (Table 2). In PD, studies have revealed that the predictors of cognitive change and progression to MCI and dementia overlap to some extent with those in the general population [57,100], but also include a distinctive set of cognitive, neurologic, psychiatric, biologic, and genetic factors that may be disease-specific, as well as factors related to the clinical severity of PD such as duration and stage [57,[100][101][102][103][104][105][106][107].…”

Section: Predictors Of Cognitive Change and Conversion To MCI And Demmentioning

confidence: 99%

Mind the gaps: What we don't know about cognitive impairment in essential tremor

Louis

Joyce

Cosentino

2019

Parkinsonism & Related Disorders

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Introduction: Although the hallmark feature of essential tremor (ET) is tremor, there is growing appreciation that cognitive impairment also occurs, including increased prevalence of mild cognitive impairment (MCI) and increased prevalence and incidence of dementia. With emerging knowledge of ET-cognitive impairment, come fundamental questions regarding its course, bases, predictors and clinical outcomes. Studies in the general population and in Parkinson's disease (PD), a related movement disorder, offer a starting point from which to begin filling these clinically important knowledge gaps. Methods: A PubMed search (June 2018) identified articles for this review. Results: Much of our knowledge of cognitive impairment in ET is of the static condition (e.g., prevalence of cognitive impairment in ET), with nearly no information on its bases, predictors and dynamics (i.e., course, and clinical outcomes). In PD, where such data have been published, rates of cognitive decline and conversion to MCI/dementia are higher than in the general population. Predictors of cognitive change in PD and the general population have also been identified, yet they only partially overlap one another.

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Cognitive functioning in individuals with Parkinson’s disease and traumatic brain injury: A longitudinal study

Cited by 9 publications

References 11 publications

White matter cortico-striatal tracts predict apathy subtypes in Huntington's disease

White matter cortico-striatal tracts predict apathy subtypes in Huntington's disease

Novel GLP-1R/GIPR co-agonist “twincretin” is neuroprotective in cell and rodent models of mild traumatic brain injury

Mind the gaps: What we don't know about cognitive impairment in essential tremor

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