Derek Burnett
Derek Burnett is a Contributing Writer at Bottom Line Personal, where he writes frequently on health and wellness. He is also a contributing editor with Reader’s Digest magazine.
Lewy Body Dementia (LBD), sometimes called Dementia with Lewy Bodies, is the third most common form of dementia (after Alzheimer’s disease and vascular dementia), affecting approximately 1.3 million American adults and accounting for up to 30% of dementia cases. Like Alzheimer’s and vascular dementia, LBD is progressive and irreversible, and is marked by mental decline. It often occurs alongside other forms of dementia.
While the key feature of Alzheimer’s pathology is the presence of amyloid plaques and neurofibrillary tangles, and while the principal characteristic of vascular dementia is blood-vessel-related damage in the brain, LBD’s distinguishing trait is the accumulation in brain cells of clusters of a microscopic protein called alpha-synuclein. When those abnormal deposits form, they’re known as Lewy bodies.
Alpha-synuclein is not normally toxic. Experts still aren’t completely sure about its usual role, but it may contribute to the process of brain cells (neurons) communicating with each other. The trouble comes when it collects into Lewy bodies, which cause irreparable damage to neurons.
LBD is most often diagnosed in people ages 65 or older. However, a 2024 study published in Annals of Neurology found that, based on autopsies of 600 people age 16 to 95 who died outside of hospital settings, nearly one in 10 people age 50 or older have the kinds of changes in their brains associated with LBD, suggesting that the disease begins to take shape much earlier than previously thought.
The first area of the brain to be affected by LBD is usually the cerebral cortex, home to such critical functions as visual processing, attention, thinking, emotion, memory, movement, and regulation of sleep. Early symptoms of LBD often include changes in alertness and ability to pay attention, drowsiness, apathy, problems sleeping, confusion, and visual hallucinations and delusions. Later, they may lose spontaneous movement. Most people will also experience memory and thinking problems similar to those typically seen in Alzheimer’s disease.
In diagnosing LBD, clinicians look for symptoms in five key areas:
Research over the past decades suggests that it makes sense to speak of “Lewy body diseases,” rather than referring to one single disease. That’s because Parkinson’s disease is also marked by the presence of Lewy bodies, and because LBD may have two distinct types.
As noted above, in LBD, Lewy bodies first form in the cerebral cortex and then may spread to other parts of the brain. In Parkinson’s, abnormal deposits first appear in a different brain region, called the substantia nigra, which controls movement. That explains the telltale Parkinson’s symptoms of balance problems, rigid muscles, slowness of movement, and tremors. As Parkinson’s progresses and other brain regions become affected, people begin to experience the other symptoms typical of LBD. And the reverse is also true—people diagnosed with LBD may, once the Lewy bodies have begun to appear in parts of the brain that control movement, begin to display Parkinson’s-like symptoms.
Leaving Parkinson’s aside, there’s reason to wonder whether LBD itself is one or two diseases, or at least whether it has two types. For most people with Lewy bodies, damage first manifests in the brainstem and then travels upward into the main structure of the brain. But studies led by researchers from Finland’s University of Helsinki show that for some, the onset of LBD occurs in the amygdala. (As you may know, the amygdala, often referred to as the “lizard brain,” regulates emotions and fear.) Those in the second group are initially affected by changes in their olfactory bulbs, which control the sense of smell, while most people experience changes in the olfactory bulb later in the disease. This may have important implications, since amygdala-based progression of LBD is usually accompanied by Alzheimer’s disease and since it more often results in dementia and tends to have an onset of 3.3 years earlier than the other subtype. These differences may be important as researchers develop therapies to treat the disease early in its progression.
Until recently, little was known about the role of genetics in LBD. But a 2021 study in Nature Genetics identified mutations on five genes that were significantly associated with the disease. The genes are:
LBD cannot be cured, nor do we yet have effective treatments for slowing its progression or halting its damage. Instead, all current LBD treatments are focused on alleviating some of the symptoms of the illness. For example, people are often treated with antidepressant medications. Some doctors prescribe cholinesterase inhibitors, drugs frequently administered to people with Alzheimer’s, to help with thinking problems. Antipsychotic drugs are sometimes tried, but they have a high rate of harmful side effects in people with LBD. And Parkinson’s medications may help to correct muscle stiffness and slowness of movement…although in many, these may worsen cognitive symptoms.
