Dementia with Lewy Bodies (DLB)

What Is Dementia with Lewy Bodies?

Dementia, recognized as a major neurocognitive disorder, is an acquired progressive mental retardation syndrome that mainly affects the elder population over 65 years old. It can be divided into several different subtypes, such as Alzheimer's disease (AD), vascular dementia, frontotemporal dementia, Lewy body dementia, etc. Among these, dementia with Lewy bodies (DLB) is a kind of Lewy body dementias characterized by Lewy bodies.

First reported in 1976, DLB now has been considered the second most common neurodegenerative disease among elder individuals. Generally, DLB progresses slowly, which presents signs of impaired memory, language, and visuospatial skills, like AD. It worsens over time, manifesting as cognitive fluctuations, rapid eye movement sleep behavior disorder, visual hallucinations, spontaneous features of parkinsonism, and eventually presenting full-blown dementia.

Risk Factors and Causes of Dementia with Lewy Bodies

Although DLB is an age-related disease mainly affecting the elderly, an array of risk factors has been revealed to associate with DLB.

1. Genetic factors: mutations in the APOE ε4, GBA, SNCA, and LRRK2 genes have been demonstrated to be possible causes of DLB.
2. Psychological factors: individuals who have been diagnosed with anxiety and depression previously are more likely to develop DLB.
3. Function impairments: it has been indicated that brain trauma, visual and auditory sensory impairment, drug abuse also ate possible risk factors for both AD and DLA.
4. Other factors: related diseases, unhealthy lifestyles such as smoking and alcoholism, air pollution, obesity, physical inactivity, education level, and so forth are all possible factors for DLB.

Critical Biomarker Molecules of Dementia with Lewy Bodies

DLB is pathologically characterized by the presentation of Lewy bodies or Lewy neurites in the brain. Under pathological conditions, the conformation of the α-synuclein protein alters, or the α-synuclein is abnormally posttranslational modified such as phosphorylated, truncated, and nitrated, resulting in reduced solubility. These α-synucleins aggregate into oligomers, or are associated with other proteins, forming Lewy bodies. These Lewy bodies, which can damage the function of neurons, are widely distributed in the cerebral cortex, brainstem, and limbic system in DLB patients.

When these Lewy bodies aggregate in large numbers on different neural pathways, corresponding functions will be affected. Such as, learning and memory functions are decreased when the cholinergic nerve is affected by these Lewy bodies; while cognitive, emotional, sleep or behavior disorders will be caused when dopaminergic pathways are blocked by Lewy bodies. Additionally, another protein amyloid-beta (Aβ) also has been indicated to play a critical role in the neuropathological pathway of DLB through the tauopathies.

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