II.P13 Amyloid load in Parkinson's Disease Dementia (PDD) and Lewy Body Dementia (LBD) measured with 11C-PIB PET

Edison, Paul; Rowe, Chris; Ahmed, Imtiaz; Villemagne, Victor L.; Rinne, Juha O.; Brooks, DJ

doi:10.1016/s1353-8020(07)70092-5

Cited by 18 publications

(20 citation statements)

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“…A recent study of PIB PET as a marker of amyloid distribution has suggested significantly raised amyloid load in over 80% of DLB subjects while amyloid pathology was infrequent in PDD (Edison et al, 2008). The clinical criteria used for diagnosing DLB and PDD clinically have been shown to have good diagnostic specificity but poorer sensitivity (McKeith et al, 2005), especially when concurrent AD pathology is present (Merdes et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia

Andersson

Zetterberg

Minthon

et al. 2010

Int J Geriat Psychiatry

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Section: Introductionmentioning

confidence: 99%

The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia

Andersson

Zetterberg

Minthon

et al. 2010

Int J Geriat Psychiatry

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“…Two out of 4 PIB-negative AD patients (7 and 8) later developed symptoms consistent with probable DLB [60] . Even if senile plaques with A ␤ are present in most DLB cases, at least 10-15% is pure DLB without A ␤ burden [9,61,62] . Both patients 9 and 10 have mainly preserved personalities and absence of disinhibition, hence, they do not fulfil the criteria of the FTD diagnosis [63] .…”

Section: Discussionmentioning

confidence: 99%

“…Further, postmortem correlates of in vivo PET PIB amyloid imaging in AD show a strong association with A ␤ plaque burden [8] . However, some patients with clinically diagnosed AD have low PIB retention [7,9] , but the reason is so far not explained, since postmortem correlates are lacking.…”

Section: Introductionmentioning

confidence: 99%

Pittsburgh Compound-B and Alzheimer’s Disease Biomarkers in CSF, Plasma and Urine: An Exploratory Study

Gunnarsson

Lindau

Wall

et al. 2010

Dement Geriatr Cogn Disord

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Background: The positron emission tomography (PET) radiotracer Pittsburgh Compound-B (PIB) is an in vivo ligand for measuring β-amyloid (Aβ) load. Associations between PET PIB and cerebrospinal fluid (CSF) Aβ1–42 and apolipoprotein E Ε4 (APOE Ε4) have been observed in several studies, but the relations between PIB uptake and other biomarkers of Alzheimer’s disease (AD) are less investigated. Method: PET PIB, PET 18Fluoro-2-deoxy-D-glucose and different AD biomarkers were measured twice in CSF, plasma and urine 12 months apart in 10 patients with a clinical diagnosis of mild to moderate AD. Results: PIB retention was constant over 1 year, inversely related to low CSF Aβ1–42 (p = 0.01) and correlated positively to the numbers of the APOE Ε4 allele (0, 1 or 2) (p = 0.02). There was a relation between mean PIB retention and CSF ApoE protein (r = –0.59, p = 0.07), and plasma cystatin C (r = –0.56, p = 0.09). Conclusion: PIB retention is strongly related to CSF Aβ1–42, and to the numbers of the APOE Ε4 allele.

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“…42 Although less frequent than in diffuse Lewy body disease (DLB), cortical Aβ aggregates can be found in approximately one-fifth of PDD patients, 43 and elevated PIB binding on PET imaging has been noted in a similar proportion of these patients. [44][45][46] Interestingly, PDD patients with and without PIB activity do not appear to differ behaviorally, 44,46 suggesting that focally increased amyloid deposition is not the cause of impaired cognitive functioning in these patients. PIB has been shown to bind to α-synuclein fibrils, although with a much lower affinity than to Aβ.…”

Section: Dopaminergic Imagingmentioning

confidence: 99%

Imaging, Cognition, and Parkinson’s Disease—An Overview

Mattis¹,

Eidelberg²

2010

US Neurology

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Parkinson's disease (PD) is characterized by motor symptoms including resting tremor, rigidity, and bradykinesia. However, cognitive and behavioral problems in PD are common 1 and can have a significant effect on quality of life. 2,3 The prevalence of dementia in patients with PD has conservatively been estimated to range between 24 and 31%. 4 The cognitive profile observed in PD patients with dementia (PDD) is substantially different from that of the primarily cortical dementia of Alzheimer's disease (AD). Patients with PDD typically exhibit difficulties with executive functions, the retrieval aspects of memory, and visuospatial skills. 4 They do not exhibit clear aphasia, apraxia, or agnosia, which are common features of AD. The onset of dementia in PD is insidious, typically occurring years after the onset of motor symptoms. However, cognitive difficulties have been observed even in early PD. 5 Although debated, the pattern of early cognitive dysfunction in PD is believed to be generally similar to that of PDD.6,7The pathophysiology of cognitive symptoms in PD is believed to be different from that of the motor symptoms. [8][9][10] Several theories exist regarding the origins of this particular clinical manifestation. It is possible that cognitive dysfunction in PD is related to the depletion of striatal dopamine and its effect on non-motor cortico-striato-pallidal- cholinergic neurotransmitter systems will be discussed, as well as findings from in vivo detection of amyloid-beta.

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II.P13 Amyloid load in Parkinson's Disease Dementia (PDD) and Lewy Body Dementia (LBD) measured with 11C-PIB PET

Cited by 18 publications

References 0 publications

The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia

The cognitive profile and CSF biomarkers in dementia with Lewy bodies and Parkinson's disease dementia

Pittsburgh Compound-B and Alzheimer’s Disease Biomarkers in CSF, Plasma and Urine: An Exploratory Study

Imaging, Cognition, and Parkinson’s Disease—An Overview

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