DLB is the second most common type of neurodegenerative type of dementia after Alzheimer’s disease (AD). It is associated with hallucinations, fluctuations in cognition and the symptoms of Parkinson’s disease (e.g. tremor, slowness, stiffness, falls).
Deposits of a protein called amyloid are a characteristic finding in the brains of people with AD. Amyloid deposits have also been found in the brains of patients with DLB. The levels of amyloid found in DLB are variable and the effect of amyloid pathology in DLB is not clear. Post-mortem studies have found links between amyloid levels and cognitive impairment, motor performance and disease progression. However, findings have not been consistent across studies. This may be due to different sample populations, small sample sizes and different measures of amyloid burden post-mortem.
Amyloid can now be measured in the brains of living people using amyloid PET scanning. A radioactive chemical that binds to amyloid is injected into the person’s vein, and the amount of the chemical that binds in their brain can then be measured. In such scans, patients with DLB have been shown to be more likely to have high levels of amyloid than healthy controls or those with Parkinson’s disease dementia, a disease closely related to DLB. This suggests that amyloid may play a role in the development and progression of dementia in DLB.
The aims of this project are to compare brain amyloid levels in patients with DLB, AD and healthy older people; and to assess the importance of amyloid burden in DLB. Study volunteers will have an amyloid PET scan at baseline, along with a thorough clinical assessment, recording the presence and severity of symptoms associated with DLB and detailed measures of cognitive function. The clinical assessment will then be repeated after one year. From previous research, we expect amyloid levels to be higher in DLB than controls, but lower than AD.
Other key questions we wish to answer are:
Do people with DLB and high brain amyloid levels have a different pattern of symptoms and cognitive deficits compared to those with low levels of amyloid?
Is the presence of amyloid in DLB associated with a more rapid disease progression at one year follow-up?