Dementia in Parkinson's disease

Martı́, Marı́a José; Tolosa, Eduardo; Cerda, Andres de la

doi:10.1007/s00415-007-5007-5

Cited by 6 publications

(5 citation statements)

References 64 publications

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“…The presence of α‐synuclein‐positive LBs was reported in 22% of familial AD cases and in 50–60% of sporadic AD cases, particularly in the amygdala (Lippa et al ., ; Hamilton, ; Wirths & Bayer, ; Swirski et al ., ), so the presence of oligomeric α‐synuclein should be expected in a substantial percentage of the AD samples. In a parallel fashion, dementia affects nearly one‐third of PD patients (Martí et al ., ), and there is an increase in cortical Aβ plaque loads in PD with dementia patients (Irwin et al ., ). Therefore a significant percentage of PD cases should show β‐amyloid pathology, as reflected here by the presence of A4‐reactive oligomeric β‐amyloid in serum.…”

Section: Discussionmentioning

confidence: 99%

Oligomeric α‐synuclein and β‐amyloid variants as potential biomarkers for Parkinson's and Alzheimer's diseases

Williams

Schulz

Sierks

2015

Eur J of Neuroscience

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Oligomeric forms of alpha-synuclein and beta-amyloid are toxic protein variants thought to contribute to the onset and progression of Parkinson’s (PD) and Alzheimer’s (AD) diseases, respectively. Detection of toxic variants in human cerebrospinal fluid (CSF) and blood has great promise to facilitate early and accurate diagnoses of these devastating diseases. Two hurdles that have impeded the use of these protein variants as biomarkers are the availability of reagents that can bind the different variants and a sensitive assay to detect their very low concentrations. We previously isolated antibody based reagents that selectively bind two different oligomeric variants of alpha-synuclein and two of beta-amyloid and developed a phage-based capture ELISA with sub-femtomolar sensitivity to quantify their presence. Here we used these reagents to show that these oligomeric alpha-synuclein variants are preferentially present in the PD brain tissue, CSF and sera and that the oligomeric beta-amyloid variants are preferentially present in the AD brain tissue, CSF and sera. Some AD samples also had alpha-synuclein pathology and some PD samples also had beta-amyloid pathology, and very intriguingly, these PD cases also had a history of dementia. Detection of different oligomeric alpha-synuclein and beta-amyloid species is an effective method to identify tissue, CSF and sera from PD and AD samples, respectively and samples which also contained early stages of other protein pathologies, indicating their potential value as blood based biomarkers for neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

Oligomeric α‐synuclein and β‐amyloid variants as potential biomarkers for Parkinson's and Alzheimer's diseases

Williams

Schulz

Sierks

2015

Eur J of Neuroscience

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“…Visual hallucinations are the most frequent psychotic symptom present in PDD [101], occurring in nearly half of patients [102]. Delusions usually in the presence of comorbid hallucinations in PDD and are seen in up to 10% of patients [103, 104].…”

Section: Psychosis Associated With Other Dementiasmentioning

confidence: 99%

“…Worsening parkinsonism with the use of antipsychotics merits careful attention, especially since sensitivity to antipsychotic medications is one of the suggestive diagnostic features of LBD [97] and dopaminergic blockade can worsen parkinsonian symptoms in both conditions. For the psychosis of PDD, RCTs indicate that low dose clozapine (25 to 150mg) is efficacious without worsening parkinsonism symptoms, although clozapine is challenging to use in older adults because of its risk for agranulocytosis (necessitating frequent lab draws) and its potent anti-cholinergic properties [101, 150, 151]. Quetiapine is anecdotally the first-line treatment for psychosis in PD, but interestingly, RCTs comparing it to placebo do not strongly support its efficacy [152, 153].…”

Section: Treatmentmentioning

confidence: 99%

New Wine in Old Bottle: Late-life Psychosis

Iglewicz

Meeks

Jeste

2011

Psychiatric Clinics of North America

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Psychosis is common in late life and exacts enormous costs to society, affected individuals, and their caregivers. A multitude of etiologies for late-life psychosis exist, the two most prototypical being schizophrenia and psychosis of Alzheimer’s Disease (AD). As such, this review will focus on the non-affective, neuropsychiatric causes of chronic psychosis in the elderly, specifically schizophrenia, delusional disorder, and the psychosis of AD and other dementias. As evidenced in this review, the current research regarding the onset and course of late-life schizophrenia reflects a more favorable prognosis than that painted by the Kraepelinian notion of schizoprenia as “dementia praecox.” Antipsychotics are useful in controlling the symptoms of late-life schizophrenia, but their use among older adults warrants increased vigilance because of older adults’ increased proclivity to side effects. Psychosocial interventions can be effective, usually in conjunction with medication. Meanwhile, psychosis of AD occurs in nearly half of people with AD and is associated with increased hospitalizations, institutionalization, caregiver distress, and mortality. Despite the profound consequences of psychotic symptoms associated with dementias, the extant literature does not afford clinicians clear, consistent guidance on how to provide optimal treatment to specific patients. Second generation antipsychotics are usually the choice treatment for psychosis, but the black box warning regarding their associated 1–2% increased absolute risk in stroke and overall mortality in patients with dementia complicates their use. Using second generation antipsychotics in low doses for brief periods and discontinuing them when possible is the best clinical practice for dementia-related psychosis. Psychosocial interventions for the treatment of psychosis with AD appear promising in empirical research, but more rigorous study is needed.

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“…Psychological and behavioral features associated with PD can include apathy, depression, visual hallucinations, delusions, and excessive daytime sleepiness [1]. Thus, diagnosis of Parkinson's disease dementia (PDD) can be complicated due to these and other issues related to medication, depression, fatigue related to sleep disturbance, and functional impairment due to motor symptoms [2]. Although patients with PD may experience cognitive deficits, the neuropsychological characteristics of PDD by nature are more severe and often include impairment in multiple domains including processing speed, working memory, and attention in addition to executive dysfunction and visual-spatial deficits [3, 4].…”

Section: Introductionmentioning

confidence: 99%

“…1 Thus, diagnosis of PD dementia (PDD) can be complicated owing to these and other issues related to medication, depression, fatigue related to sleep disturbance, and functional impairment resulting from motor symptoms. 2 Although patients with PD may experience cognitive deficits, the neuropsychological characteristics of PDD by nature are more severe and often include impairment in multiple domains, including processing speed, working memory, and attention in addition to executive dysfunction and visual-spatial deficits. 3,4 In 2007, the International Parkinson and Movement Disorder Society (MDS) Task Force published guidelines for diagnosing PDD, which requires diagnosis of PD based on Queen Square Brain Bank criteria, slowly progressive decline from premorbid levels, impairment in more than one cognitive domain, at least one behavioral feature, and significant functional impairment independent of motor symptoms.…”

mentioning

confidence: 99%

Development of Clinical Dementia Rating Scale Cut‐off Scores for Patients With Parkinson's Disease

Wyman‐Chick

Scott

2015

Movement Disord Clin Pract

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Background The purpose of this study was to explore validity of the Clinical Dementia Rating Scale in measuring cognitive impairment among individuals with Parkinson's disease. The scale was created for use in patients with Alzheimer's disease and, to date, there have been no published studies examining if this tool is appropriate for patients with Parkinson's disease. Methods The data were obtained from the National Alzheimer's Coordinating Center database and included 490 subjects diagnosed with Parkinson's disease, further categorized as having Parkinson's disease dementia (n= 151), mild cognitive impairment (n= 186), or normal cognition (n = 153) by a treating physician. Sensitivity, specificity, positive predictive value and negative predictive values were calculated for the Clinical Dementia Rating Scale Global Score as well as the Sum of Boxes Score using existing cutoff scores. Finally, new cutoff scores were calculated using sensitivity and specificity values derived using Receiver Operating Characteristic curves. Results Sensitivity and specificity of the published Global Score cutoff scores for patients with dementia were .34 and .10, respectively. The newly calculated cutoff scores for patients with dementia yielded a sensitivity of .79 and a specificity of .96. The area under the curve was 0.92 (95% CI = 0.90-0.95). Conclusion The CDR is a useful tool in identifying dementia in patients with Parkinson's disease when the cutoff scores are adjusted.

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Dementia in Parkinson's disease

Cited by 6 publications

References 64 publications

Oligomeric α‐synuclein and β‐amyloid variants as potential biomarkers for Parkinson's and Alzheimer's diseases

Oligomeric α‐synuclein and β‐amyloid variants as potential biomarkers for Parkinson's and Alzheimer's diseases

New Wine in Old Bottle: Late-life Psychosis

Development of Clinical Dementia Rating Scale Cut‐off Scores for Patients With Parkinson's Disease

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