New research may help physicians to more quickly and accurately diagnose dementia with Lewy bodies (DLB), one of the clinical diagnoses grouped under the umbrella term Lewy body dementias (LBD). Currently, physicians diagnose LBD based on the presence of clinical features only, as there are no widely available biological tests that can confirm the clinical diagnosis.
Clinical symptoms of DLB include fluctuating cognition, visual hallucinations, and parkinsonism along with rapid eye movement sleep disorders, neuroleptic sensitivity, and an abnormal test result of brain imaging to detect dopamine levels. (This test is not yet widely available.) Because of the difficulty in assessing clinical features, people with LBD often must make multiple visits to several physicians before receiving a correct diagnosis. The availability of a clinical test for LBD would greatly benefit both patients and caregivers.
Dr. James Galvin and a team at Washington University in St. Louis studied levels of several proteins in cerebrospinal fluid, including amyloid-beta42 and tau, which are linked to Alzheimer’s disease, and alpha-synuclein, which is linked to Lewy body dementias. The cerebrospinal fluid of 33 patients (11 with DLB, 11 with Alzheimer’s disease, and 11 controls) was studied. Alpha-synuclein levels were found to be lowest in people with DLB and amyloid-beta42 levels were lowest in people with Alzheimer’s. However, levels of tau protein were not useful in differentiating between DLB and Alzheimer’s disease.
Of special interest, the researchers noted that the biomarkers were not only accurate in identifying the patients’ specific conditions, but also were able to identify 3 people in the control group whose low alpha-synuclein levels indicated they had pre-clinical DLB and who later developed possible DLB (2 people) and probable DLB (1 person) during the study’s follow-up period. In addition, the researchers found that patients with low levels of both alpha-synuclein and amyloid-beta42 showed evidence of having both DLB and Alzheimer’s and who performed worse on memory tests than those who only had low levels of either alpha-synuclein or amyloid-beta42. (The majority of people with DLB, as high as 80%, have some level of Alzheimer’s changes in the brain; up to 35% of people with Alzheimer’s disease have some Lewy body pathology as well.)