Special Issue "Parkinson’s Disease and Cognition"

A special issue of Behavioral Sciences (ISSN 2076-328X). This special issue belongs to the section "Cognition".

Deadline for manuscript submissions: closed (31 May 2021).

Special Issue Editor

Dr. Carmen Gasca-Salas
E-Mail Website
Guest Editor
1. - Centro Integral en Neurociencias A.C. (CINAC), HM Hospitales- Puerta del Sur. CEU-San Pablo University, Madrid, Spain
2. CIBERNED
Interests: Parkinson’s disease; movement disorders; neurodegenerative diseases; cognitive impairment and dementia; neurodegeneration; neuroimaging; clinical neuropsychology; neurological diseases

Special Issue Information

Dear Colleagues,

It is my pleasure to announce a new Special Issue of Behavioral Sciences on “Cognition in Parkinson’s Disease”. Since the recognition of nonmotor symptoms in Parkinson’s disease, cognitive impairment has attracted a lot of interest, mainly due to its impact on quality of life and daily function. It affects a high number of patients, keeping in mind that Parkinson’s disease is the second most common neurodegenerative disease after Alzheimer’s disease and that up to 80% of patients will develop it in the long term.

Even though there are still unmet needs, such as an specific an effective treatment, knowledge about this entity has increased in the last few years. I would like to invite you to collaborate in this Special Issue, including helpful information for the readers such as the epidemiology and importance of mild cognitive impairment and dementia and PD, how to make the diagnosis and which tests we should use, biomarkers including CSF and neuroimaging, as well as current treatments, drugs in development, and potential future approaches. I would also like to include the clinical semiology describing the different cognitive domains including also social cognition, a less studied field in PD but with a huge interest in social interactions in these patients.  

A better recognition and approach of this disabling entity may have a huge beneficial effect on our patients.

I hope you find this project interesting, and I will be so glad if you agree to collaborate with us.  

Dr. Carmen Gasca-Salas
Guest Editor

Manuscript Submission Information

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Keywords

  • Parkinson’s disease
  • Mild cognitive impairment
  • Dementia
  • Treatment
  • Neuroimaging

Published Papers (4 papers)

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Review

Review
What Do We Know about Theory of Mind Impairment in Parkinson’s Disease?
Behav. Sci. 2021, 11(10), 130; https://0-doi-org.brum.beds.ac.uk/10.3390/bs11100130 - 24 Sep 2021
Viewed by 351
Abstract
Theory of mind (ToM) is a social cognitive skill that involves the ability to attribute mental states to self and others (what they think (cognitive ToM) and feel (affective ToM)). We aim to provide an overview of previous knowledge of ToM in Parkinson’s [...] Read more.
Theory of mind (ToM) is a social cognitive skill that involves the ability to attribute mental states to self and others (what they think (cognitive ToM) and feel (affective ToM)). We aim to provide an overview of previous knowledge of ToM in Parkinson’s disease (PD). In the last few years more attention has been paid to the study of this construct as a non-motor manifestation of PD. In advanced stages, both components of ToM (cognitive and affective) are commonly impaired, although in early PD results remain controversial. Executive dysfunction correlates with ToM deficits and other cognitive domains such as language and visuospatial function have also been related to ToM. Recent studies have demonstrated that PD patients with mild cognitive impairment show ToM deficits more frequently in comparison with cognitively normal PD patients. In addition to the heterogeneity of ToM tests administered in different studies, depression and dopaminergic medication may also be acting as confounding factors, but there are still insufficient data to support this. Neuroimaging studies conducted to understand the underlying networks of cognitive and affective ToM deficits in PD are lacking. The study of ToM deficit in PD continues to be important, as this may worsen quality of life and favor social stigma. Future studies should be considered, including assessment of the patients’ cognitive state, associated mood disorders, and the role of dopaminergic deficit. Full article
(This article belongs to the Special Issue Parkinson’s Disease and Cognition)
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Review
Lewy Body Dementias: A Coin with Two Sides?
Behav. Sci. 2021, 11(7), 94; https://0-doi-org.brum.beds.ac.uk/10.3390/bs11070094 - 22 Jun 2021
Cited by 1 | Viewed by 1097
Abstract
Lewy body dementias (LBDs) consist of dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), which are clinically similar syndromes that share neuropathological findings with widespread cortical Lewy body deposition, often with a variable degree of concomitant Alzheimer pathology. The objective of [...] Read more.
Lewy body dementias (LBDs) consist of dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), which are clinically similar syndromes that share neuropathological findings with widespread cortical Lewy body deposition, often with a variable degree of concomitant Alzheimer pathology. The objective of this article is to provide an overview of the neuropathological and clinical features, current diagnostic criteria, biomarkers, and management of LBD. Literature research was performed using the PubMed database, and the most pertinent articles were read and are discussed in this paper. The diagnostic criteria for DLB have recently been updated, with the addition of indicative and supportive biomarker information. The time interval of dementia onset relative to parkinsonism remains the major distinction between DLB and PDD, underpinning controversy about whether they are the same illness in a different spectrum of the disease or two separate neurodegenerative disorders. The treatment for LBD is only symptomatic, but the expected progression and prognosis differ between the two entities. Diagnosis in prodromal stages should be of the utmost importance, because implementing early treatment might change the course of the illness if disease-modifying therapies are developed in the future. Thus, the identification of novel biomarkers constitutes an area of active research, with a special focus on α-synuclein markers. Full article
(This article belongs to the Special Issue Parkinson’s Disease and Cognition)
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Review
Cognitive Impairment in Parkinson’s Disease: Epidemiology, Clinical Profile, Protective and Risk Factors
Behav. Sci. 2021, 11(5), 74; https://0-doi-org.brum.beds.ac.uk/10.3390/bs11050074 - 13 May 2021
Cited by 1 | Viewed by 1164
Abstract
Cognitive impairment is a common non-motor symptom in Parkinson’s Disease (PD) and an important source of patient disability and caregiver burden. The timing, profile and rate of cognitive decline varies widely among individuals with PD and can range from normal cognition to mild [...] Read more.
Cognitive impairment is a common non-motor symptom in Parkinson’s Disease (PD) and an important source of patient disability and caregiver burden. The timing, profile and rate of cognitive decline varies widely among individuals with PD and can range from normal cognition to mild cognitive impairment (PD-MCI) and dementia (PDD). Beta-amyloid and tau brain accumulation, oxidative stress and neuroinflammation are reported risk factors for cognitive impairment. Traumatic brain injury and pesticide and tobacco exposure have also been described. Genetic risk factors including genes such as COMT, APOE, MAPT and BDNF may also play a role. Less is known about protective factors, although the Mediterranean diet and exercise may fall in this category. Nonetheless, there is conflicting evidence for most of the factors that have been studied. The use of inconsistent criteria and lack of comprehensive assessment in many studies are important methodological issues. Timing of exposure also plays a crucial role, although identification of the correct time window has been historically difficult in PD. Our understanding of the mechanism behind these factors, as well as the interactions between gene and environment as determinants of disease phenotype and the identification of modifiable risk factors will be paramount, as this will allow for potential interventions even in established PD. Full article
(This article belongs to the Special Issue Parkinson’s Disease and Cognition)
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Review
Treatment of Parkinson’s Disease with Cognitive Impairment: Current Approaches and Future Directions
Behav. Sci. 2021, 11(4), 54; https://0-doi-org.brum.beds.ac.uk/10.3390/bs11040054 - 17 Apr 2021
Cited by 1 | Viewed by 1162
Abstract
Cognitive impairment risk in Parkinson’s disease increases with disease progression and poses a significant burden to the patients, their families and society. There are no disease-modifying therapies or preventative measures for Parkinson’s disease mild cognitive impairment (PD-MCI), or Parkinson’s disease dementia (PDD). This [...] Read more.
Cognitive impairment risk in Parkinson’s disease increases with disease progression and poses a significant burden to the patients, their families and society. There are no disease-modifying therapies or preventative measures for Parkinson’s disease mild cognitive impairment (PD-MCI), or Parkinson’s disease dementia (PDD). This article reviews current and previously investigated treatments and those under investigation, including pharmacologic, non-pharmacologic and surgical procedures. There are currently no effective pharmacologic or non-pharmacologic treatments for PD-MCI. The only recommended treatment for PDD currently is rivastigmine, a cholinesterase inhibitor. Donepezil and galantamine—other cholinesterase inhibitors—are possibly useful. Memantine, a N-methyl-D-aspartate (NMDA) receptor antagonist, is considered investigational in PDD. Drug repurposing (atomoxetine, levodopa, insulin, atomoxetine for PD-MCI; ambroxol and ceftriaxone for PDD) and novel medications (SYN120, GRF6021, NYX-458 for PD-MCI; ANAVEX2-73, LY3154207, ENT-01, DAAOI-P for PDD) currently have insufficient evidence. There is growing research supporting exercise in the treatment of PD-MCI, but most non-pharmacological approaches have insufficient evidence for use in PD-MCI (cognitive rehabilitation, deep brain stimulation, transcranial direct current stimulation, transcranial ultrasound, vestibular nerve stimulation) and PDD (cognitive intervention, deep brain stimulation, transcranial alternating current stimulation, transcranial ultrasound, temporal blood brain barrier disruption). Research is needed for both disease-modifying and symptomatic treatments in PD cognitive impairment. Full article
(This article belongs to the Special Issue Parkinson’s Disease and Cognition)
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