Spatial attention and spatial short term memory in PSP and Parkinson's disease

Smith, Daniel T.; Casteau, Soazig; Archibald, Neil

doi:10.1016/j.cortex.2020.12.019

Cited by 11 publications

(14 citation statements)

References 78 publications

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“…In addition to the symptoms associated with motor disorders, so-called non-motor disorders are observed in patients with parkinsonism, among which cognitive dysfunctions are the most common [ 80 , 81 , 82 ]. In particular, a large number of papers describing the pathological phenotype of Parkinson’s disease in both humans and animal models indicate an impairment of hippocampus-dependent spatial memory [ 83 , 84 , 85 ]. As part of our study in the Y-shaped maze test, mice receiving rotenone spent significantly less time in the correct maze arm, which indicates their impaired ability to learn and form memory.…”

Section: Discussionmentioning

confidence: 99%

Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson’s Disease Model by Alleviating Mitochondrial Dysfunction

Aleksandrova

Chaprov

Podturkina

et al. 2023

IJMS

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Parkinson’s disease is the second most common neurodegenerative disease. Unfortunately, there is still no definitive disease-modifying therapy. In our work, the antiparkinsonian potential of trans-epoxide (1S,2S,3R,4S,6R)-1-methyl-4-(prop-1-en-2-yl)-7-oxabicyclo [4.1.0]heptan-2,3-diol (E-diol) was analyzed in a rotenone-induced neurotoxicity model using in vitro, in vivo and ex vivo approaches. It was conducted as part of the study of the mitoprotective properties of the compound. E-diol has been shown to have cytoprotective properties in the SH-SY5Y cell line exposed to rotenone, which is associated with its ability to prevent the loss of mitochondrial membrane potential and restore the oxygen consumption rate after inhibition of the complex I function. Under the conditions of rotenone modeling of Parkinson’s disease in vivo, treatment with E-diol led to the leveling of both motor and non-motor disorders. The post-mortem analysis of brain samples from these animals demonstrated the ability of E-diol to prevent the loss of dopaminergic neurons. Moreover, that substance restored functioning of the mitochondrial respiratory chain complexes and significantly reduced the production of reactive oxygen species, preventing oxidative damage. Thus, E-diol can be considered as a new potential agent for the treatment of Parkinson’s disease.

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Section: Discussionmentioning

confidence: 99%

Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson’s Disease Model by Alleviating Mitochondrial Dysfunction

Aleksandrova

Chaprov

Podturkina

et al. 2023

IJMS

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“…PSP's sequential deficits were reported in previous studies but were usually attributed to executive dysfunction or attention/working memory damages (Goel & Vyas, 2019; Smith et al., 2021). Nevertheless, the characteristic was not specified.…”

Section: Discussionmentioning

confidence: 63%

Impaired sequence manipulation in non‐demented patients with progressive supranuclear palsy

Zhang,

Ma,

Chan

et al. 2024

Brain and Behavior

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PurposeSequential working memory is the ability to maintain and manipulate sequential information at a second time scale. Patients with progressive supranuclear palsy (PSP) or Parkinson's disease (PD) perform poorly in tests that require the flexible arrangement of thoughts or actions. This study investigated whether sequential working memory is differently impaired in patients with PSP versus PD.MethodTwenty‐nine patients with PSP Richardson's syndrome (PSP‐RS), 36 patients with PD, and 36 healthy controls (HC) completed 3 well‐established neuropsychological tests, including digit span forward (DST‐F), digit span backward (DST‐B), and adaptive digit ordering tests (DOT‐A). The DST‐F required maintaining digit sequences, and the DST‐B and DOT‐A required maintaining and manipulating digit sequences.FindingThe PSP‐RS group scored lower than the PD and HC groups in the DST‐B and DOT‐A but not in the DST‐F, indicating that the ability to manipulate sequences was impaired, but the maintenance ability was preserved in PSP‐RS patients. Moreover, in PSP‐RS, the DST‐B score negatively correlated with the severity of motor symptoms. The actual levodopa dose positively correlated with the DST‐B ordering cost (DST‐F score vs. DST‐B score). The PSP patients who took a greater dose of levodopa tended to have higher DST‐B ordering cost. There was no effect of levodopa on DST‐B or DOT‐A in PD.ConclusionThese results suggested that the ability to manipulate sequence was already reduced in patients with PSP‐RS and was worse than in patients with PD.

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“…In PSP, slow eye movement saccades are sensitive indicators of the underlying disease processes, and occulomotor impairments have been shown to be closely related to the impairment of spatial attention and spatial short-term memory. 55 , 56 Although a simple clinical examination of eye movements is very likely to miss subtle saccadic slowing, this study indicates that such an examination may nonetheless capture an increased risk of cognitive decline. Recent studies have also found that brain neuroinflammation is associated with the severity of symptoms in PSP.…”

Section: Discussionmentioning

confidence: 79%

Prediction and early biomarkers of cognitive decline in Parkinson disease and atypical parkinsonism: a population-based study

Bäckström

Granåsen

et al. 2022

Brain Communications

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The progression of cognitive decline is heterogeneous in the three most common idiopathic parkinsonian diseases: Parkinson disease, multiple system atrophy and progressive supranuclear palsy. The causes for this heterogeneity are not fully understood, and there are no validated biomarkers that can accurately identify patients who will develop dementia and when. In this population-based, prospective study, comprehensive neuropsychological testing was performed repeatedly in new-onset, idiopathic parkinsonism. Dementia was diagnosed until 10 years and participants (N = 210) were deeply phenotyped by multimodal clinical, biochemical, genetic and brain imaging measures. At baseline, before the start of dopaminergic treatment, mild cognitive impairment was prevalent in 43.4% of the patients with Parkinson disease, 23.1% of the patients with multiple system atrophy and 77.8% of the patients with progressive supranuclear palsy. Longitudinally, all three diseases had a higher incidence of cognitive decline compared with healthy controls, but the types and severity of cognitive dysfunctions differed. In Parkinson disease, psychomotor speed and attention showed signs of improvement after dopaminergic treatment, while no such improvement was seen in other diseases. The 10-year cumulative probability of dementia was 54% in Parkinson disease and 71% in progressive supranuclear palsy, while there were no cases of dementia in multiple system atrophy. An easy-to-use, multivariable model that predicts the risk of dementia in Parkinson disease within 10 years with high accuracy (area under the curve: 0.86, P < 0.001) was developed. The optimized model adds CSF biomarkers to four easily measurable clinical features at baseline (mild cognitive impairment, olfactory function, motor disease severity and age). The model demonstrates a highly variable but predictable risk of dementia in Parkinson disease, e.g. a 9% risk within 10 years in a patient with normal cognition and CSF amyloid-β42 in the highest tertile, compared with an 85% risk in a patient with mild cognitive impairment and CSF amyloid-β42 in the lowest tertile. Only small or no associations with cognitive decline were found for factors that could be easily modifiable (such as thyroid dysfunction). Risk factors for cognitive decline in multiple system atrophy and progressive supranuclear palsy included signs of systemic inflammation and eye movement abnormalities. The predictive model has high accuracy in Parkinson disease and might be used for the selection of patients into clinical trials or as an aid to improve the prevention of dementia.

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Spatial attention and spatial short term memory in PSP and Parkinson's disease

Cited by 11 publications

References 78 publications

Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson’s Disease Model by Alleviating Mitochondrial Dysfunction

Monoterpenoid Epoxidiol Ameliorates the Pathological Phenotypes of the Rotenone-Induced Parkinson’s Disease Model by Alleviating Mitochondrial Dysfunction

Impaired sequence manipulation in non‐demented patients with progressive supranuclear palsy

Prediction and early biomarkers of cognitive decline in Parkinson disease and atypical parkinsonism: a population-based study

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