"Why Does Lewy Body Dementia Differ from Patient to Patient?" A Decade-Long Mystery Solved [Health Check]

[Financial News]  The mystery behind the varying symptoms and disease progression seen in patients with Lewy body dementia has been solved. A Korean research team has established that the disease progresses along two distinct pathways, opening up the possibility of personalized treatment.
A research team led by Seok Jong Chung of the Department of Neurology at Severance Hospital and Chan Wook Park of the Department of Physiology at Yonsei University College of Medicine announced on the 15th that Lewy body dementia can be divided into two progression patterns, depending on whether amyloid accumulation or degeneration of the dopaminergic system appears first. The findings were published in Brain, an international journal of neuroscience with an impact factor of 12.6.
Lewy body dementia is one of the most common neurodegenerative dementias after Alzheimer's disease (AD). It can cause visual hallucinations, REM sleep behavior disorder, and fluctuations in cognitive function. Even among patients with the same condition, symptoms and disease progression can vary considerably. In the brains of patients with Lewy body dementia, dopamine deficiency in the basal ganglia, reduced cerebral function, and beta-amyloid accumulation have been observed. However, the order in which these changes occur and progress has not been clearly established.
The research team analyzed amyloid accumulation, cerebral perfusion, and the degree of dopamine deficiency in the basal ganglia using amyloid positron emission tomography (PET) and dopamine transporter PET scans from 83 patients with Lewy body dementia. The researchers then used artificial-intelligence analysis to examine the sequence in which these brain changes appeared and estimate the disease's progression pathways.
The progression of Lewy body dementia was broadly divided into two patterns. In the first, amyloid accumulation appeared first, followed by reduced cerebral perfusion and then dopamine deficiency in the basal ganglia. In the second, dopamine deficiency in the basal ganglia occurred first, followed by reduced cerebral perfusion and amyloid accumulation.
The two patterns differed clearly not only in the sequence of disease progression but also in clinical symptoms and brain-imaging findings. Patients in whom amyloid accumulation began first showed brain atrophy resembling that seen in AD, along with high levels of amyloid accumulation. By contrast, REM sleep behavior disorder and visual hallucinations were more common among patients whose dopamine deficiency began first. They also showed more pronounced imaging features typical of Lewy body dementia, in which certain areas of the brain are relatively preserved.
Professor Chung said, "This study confirmed that Lewy body dementia can be divided into a type in which amyloid pathology progresses first and another in which degeneration of the dopaminergic system occurs first." He added, "These findings will not only provide important evidence for understanding why symptoms and disease progression differ among patients, but may also be used to develop personalized treatments and design clinical trials that take patients' pathological characteristics into account."




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