When does cerebral β‐amyloid deposition begin in Lewy body dementia?

Fujishiro, Hiroshige; Kosaka, Kenji

doi:10.1111/ncn3.12372

Cited by 3 publications

(8 citation statements)

References 66 publications

(165 reference statements)

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“…In previous pathological studies, patients with DLB showed a higher burden or phase of amyloid pathology than those with PD. [4][5][6][7][8] Another in vivo 11 C-labeled Pittsburgh compound B ( 11 C-PiB)-PET study found increased amyloid load in patients with DLB, particularly in the frontal and cingulate cortices, whereas 11 C-PiB uptake was infrequent or less in those with PD. 1,9,10 Similarly, our amyloid PET imaging showed that the DLB group had a higher burden of amyloid accumulation than the PD group in all cortical areas.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to Lewy body pathology, concomitant Alzheimer's disease (AD) pathology is commonly observed in LBD, and clinicopathological studies have shown that 30% to 40% of patients with PD and up to 70% of patients with DLB have comorbid amyloid pathology 1‐3 . Generally, the prevalence and severity of amyloid pathology are higher in patients with DLB than in patients with PD or PD dementia (PDD) 4‐8 . In vivo amyloid positron emission tomography (PET) studies have also shown that the burden of amyloid was higher in the DLB group than in the PD and PDD groups 9‐11 .…”

mentioning

confidence: 99%

“…PD or PD dementia (PDD). [4][5][6][7][8] In vivo amyloid positron emission tomography (PET) studies have also shown that the burden of amyloid was higher in the DLB group than in the PD and PDD groups. [9][10][11] Amyloid accumulation in LBDs exhibits an AD-like pattern 11 or a unique occipital cortex binding pattern.…”

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confidence: 99%

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Effect of Amyloid on Cognitive Performance in Parkinson's Disease and Dementia with Lewy Bodies

et al. 2022

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Background Concomitant amyloid pathology contributes to the clinical heterogeneity of Lewy body diseases (LBDs). Objective The objective of this study was to investigate the pattern and effect of amyloid accumulation on cognitive dysfunction in Parkinson's disease (PD) and dementia with Lewy bodies (DLB). Methods We retrospectively assessed 205 patients with LBD (91 with DLB and 114 with PD) who underwent 18F‐florbetaben positron emission tomography and divided them into amyloid‐positive and amyloid‐negative groups depending on global standardized uptake value ratios (SUVRs). We investigated the effect of group on the regional and global SUVRs using general linear models (GLMs) after controlling for age, sex, cognitive status, and score on the Korean version of the Mini‐Mental State Examination. Moreover, the effect of amyloid on cognitive function, depending on the type of LBD, was evaluated using GLMs with interaction analysis. Results In all evaluated regions including the striatum, the DLB group showed a higher SUVR than the PD group. Among amyloid‐positive patients, the DLB group had a higher regional SUVR than the PD group in the frontal and parietal cortices. There was a significant interaction effect between amyloid and disease groups in language and memory function. In patients with PD, global amyloid load was negatively associated with language (B = −2.03; P = 0.010) and memory functions (B = −1.96; P < 0.001). However, amyloid load was not significantly associated with cognitive performance in the DLB group. Conclusions Although the burden of amyloid was higher in the DLB group, amyloid accumulation was negatively associated with the memory and language functions in the PD group only. © 2022 International Parkinson and Movement Disorder Society.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

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Effect of Amyloid on Cognitive Performance in Parkinson's Disease and Dementia with Lewy Bodies

et al. 2022

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“…No clear definition of Lewy body disease as a clinical term Based on current clinical diagnostic criteria, LBD consists of DLB and Parkinson's disease (PD). 1,26,27 Longitudinal follow-up studies have revealed that most patients with isolated RBD developed DLB or PD, and, in rare cases, multiple system atrophy. Therefore, isolated RBD is proposed to be included as another clinical phenotype of LBD.…”

Section: Terminology Regarding Lewy Body Diseasementioning

confidence: 99%

“…Recent advances in understanding of the prodromal stages indicate a wider clinical spectrum of LBD according to prodromal diagnostic criteria. 14,[26][27][28][29] Considering the lack of a clear definition of LBD beyond a generic term, LBD is used as the pathological term to avoid confusion with the clinical term in this article.…”

Section: Terminology Regarding Lewy Body Diseasementioning

confidence: 99%

Clinical presentations and diagnostic application of proposed biomarkers in psychiatric‐onset prodromal dementia with Lewy bodies

Kobayashi,

Iwata‐Endo,

Fujishiro

2024

Psychogeriatrics

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Research criteria for the diagnosis of prodromal dementia with Lewy bodies (DLB) include three clinical subtypes: mild cognitive impairment with Lewy bodies (MCI‐LB), delirium‐onset prodromal DLB, and psychiatric‐onset prodromal DLB. Late‐onset psychiatric manifestations are at a higher risk of developing dementia, but its relation to prodromal DLB remains unclear. In addition to the risk of severe antipsychotic hypersensitivity reactions, accurate discrimination from non‐DLB cases is important due to the potential differences in management and prognosis. This article aims to review a rapidly evolving psychiatric topic and outline clinical pictures of psychiatric‐onset prodromal DLB, including the proposed biomarker findings of MCI‐LB: polysomnography‐confirmed rapid eye movement sleep behaviour disorder, cardiac [123I]metaiodobenzylguanidine scintigraphy, and striatal dopamine transporter imaging. We first reviewed clinical pictures of patients with autopsy‐confirmed DLB. Regarding clinical reports, we focused on the patients who predominantly presented with psychiatric manifestations and subsequently developed DLB. Thereafter, we reviewed clinical studies regarding the diagnostic applications of the proposed biomarkers to patients with late‐onset psychiatric disorders. Clinical presentations were mainly late‐onset depression and psychosis; however, other clinical manifestations were also reported. Psychotropic medications before a DLB diagnosis may cause extrapyramidal signs, and potentially influences the proposed biomarker findings. These risks complicate clinical manifestation interpretation during the management of psychiatric symptoms. Longitudinal follow‐up studies with standardised evaluations until conversion to DLB are needed to investigate the temporal trajectories of core features and proposed biomarker findings. In patients with late‐onset psychiatric disorders, identification of patients with psychiatric‐onset prodromal DLB provides the opportunity to better understanding the distinct prognostic subgroup that is at great risk of incident dementia. Advances in the establishment of direct biomarkers for the detection of pathological α‐synuclein may encourage reorganising the phenotypic variability of prodromal DLB.

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