The National Institutes of Health (nih.gov) has several publications on neurological diseases. I recently came across their booklet on “The Dementias,” which includes a short section on synucleinopathies. Synucleinopathies are caused by the abnormal accumulation of the protein alpha-synuclein. Lewy body dementia is addressed along with its two types — Dementia with Lewy bodies and Parkinson’s disease dementia.
Here are excerpts from the synucleinopathies section. Look at the booklet online for other chapters — risk factors, diagnosis and treatment, etc. — and other types of dementia.
Robin
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nia.nih.gov/alzheimers/publication/dementias/types-dementia
Excerpts from
The Dementias
NIH Online Booklet
Published September 2013 (Last Updated July 2016)
Types of Dementia
Various disorders and factors contribute to the development of dementia. Neurodegenerative disorders such as AD, frontotemporal disorders, and Lewy body dementia result in a progressive and irreversible loss of neurons and brain functions. Currently, there are no cures for these progressive neurodegenerative disorders.
Some types of dementia disorders are described below.
Synucleinopathies
In these brain disorders, a protein called alpha-synuclein accumulates inside neurons. Although it is not fully understood what role this protein plays, changes in the protein and/or its function have been linked to Parkinson’s disease and other disorders.
One type of synucleinopathy, Lewy body dementia, involves protein aggregates called Lewy bodies, balloon-like structures that form inside of nerve cells. The initial symptoms may vary, but over time, people with these disorders develop very similar cognitive, behavioral, physical, and sleep-related symptoms. Lewy body dementia is one of the most common causes of dementia, after Alzheimer’s disease and vascular disease. Types of Lewy body dementia include:
* Dementia with Lewy bodies (DLB), one of the more common forms of progressive dementia. Symptoms such as difficulty sleeping, loss of smell, and visual hallucinations often precede movement and other problems by as long as 10 years, which consequently results in DLB going unrecognized or misdiagnosed as a psychiatric disorder until its later stages. Neurons in the substantia nigra that produce dopamine die or become impaired, and the brain’s outer layer (cortex) degenerates. Many neurons that remain contain Lewy bodies.
Later in the course of DLB, some signs and symptoms are similar to AD and may include memory loss, poor judgment, and confusion. Other signs and symptoms of DLB are similar to those of Parkinson’s disease, including difficulty with movement and posture, a shuffling walk, and changes in alertness and attention. Given these similarities, DLB can be very difficult to diagnose. There is no cure for DLB, but there are drugs that control some symptoms. The medications used to control DLB symptoms can make motor function worse or exacerbate hallucinations.
* Parkinson’s disease dementia (PDD), a clinical diagnosis related to DLB that can occur in people with Parkinson’s disease. PDD may affect memory, social judgment, language, or reasoning. Autopsy studies show that people with PDD often have amyloid plaques and tau tangles similar to those found in people with AD, though it is not understood what these similarities mean. A majority of people with Parkinson’s disease develop dementia, but the time from the onset of movement symptoms to the onset of dementia symptoms varies greatly from person to person. Risk factors for developing PDD include the onset of Parkison’s-related movement symptoms followed by mild cognitive impairment and REM sleep behavior disorder, which involves having frequent nightmares and visual hallucinations.