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This case report aims to illustrate the coexistence of amyloid pathology in a patient diagnosed with dementia with Lewy bodies and rapid eye movement sleep behavior disorder.

May 17, 2026Open Access

Coexisting Amyloid Positivity and Probable Dementia With Lewy Bodies in a Patient With Rapid Eye Movement Sleep Behavior Disorder

Key Points

This case report aims to illustrate the coexistence of amyloid pathology in a patient diagnosed with dementia with Lewy bodies and rapid eye movement sleep behavior disorder.
Case report involving a 69-year-old woman with a history of RBD and cognitive decline.
Dopamine transporter PET imaging and polysomnography were performed for diagnosis confirmation.
Magnetic resonance imaging evaluated cerebral microbleeds and amyloid positron emission tomography assessed amyloid deposition.
The patient was diagnosed with dementia with Lewy bodies based on clinical presentation and imaging findings.
Amyloid PET imaging revealed diffuse cortical amyloid deposition, indicating concurrent amyloid pathology.
Polysomnography confirmed the loss of muscle atonia during REM sleep, consistent with RBD.

Abstract

Rare coexistence of disease or pathology Background:Rapid eye movement (REM) sleep behavior disorder (RBD) is a REM-related parasomnia in which the normal muscle atonia of REM sleep is lost, leading to complex motor behaviors or dream enactments.RBD is increasingly recognized as a prodromal manifestation of neurodegenerative a-synucleinopathy.It is well established in longitudinal studies that isolated RBD is among the strongest predictors of a-synucleinopathies, with more than 80-90% of patients eventually converting to Parkinson disease, dementia with Lewy bodies (DLB), or multiple system atrophy. Case Report:We report a 69-year-old woman with a previous history of RBD who was admitted for progressive cognitive and behavioral deterioration after starting antiseizure and antipsychotic medications.On admission, she exhibited bradykinesia and rigidity and dopamine transporter positron emission tomography (PET) imaging demonstrated reduced uptake in the putamina.During hospitalization, dream-enacting behaviors were observed, leading to the decision to conduct polysomnography, which confirmed loss of muscle atonia during REM sleep.Taken together, these findings supported a diagnosis of DLB and RBD.In addition, brain magnetic resonance imaging with susceptibility-weighted sequences revealed multiple cortical microbleeds consistent with cerebral amyloid angiopathy, prompting amyloid PET imaging, which showed diffuse cortical amyloid deposition and indicated concurrent amyloid pathology. Conclusions:This case highlights that RBD and characteristic neuroimaging findings are consistent with DLB as the primary disease, with coexisting amyloid pathology.Additionally, the potential influence of clinical confounders such as cerebral amyloid angiopathy, seizure, and medication effects must be taken into account.

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