2019 International LBD Conference: Overview

Last week was about the helpful programs and projects we learned about at the conference. This week a review of 142 abstracts gives us a general overview of they kinds of information presented at the conference. About half were scientific and half were clinical.

The scientists focused on biomarker identification in early LBD and in comparing LBD and AD brain pathology. The focus has definitely shifted from finding new ways to treat dementia to finding ways to identify it as early as possible. Mild cognitive impairment (MCI) was a much mentioned phrase and many reports were about efforts to identify and compare early symptoms in those with various kinds of MCI. Another strong area of focus is the identification of mixed dementias. One report noted that identifying the differences between DLB-AD and 'pure' DLB was equally or even more important than  identifying the difference between DLB and PDD.

Of the LBD symptoms, hallucinations, parkinsonism, RBD (Active Dreams), cognitive fluctuations and depression were the most discussed.

Hallucinations and visuospatial dysfunctions (poor hand-eye co-ordination, poor depth perception) were found to be associated with orthostatic hypotension (low blood pressure on rising) and slow cognition. People who hallucinated were found to put more emphasis on prior knowledge than they did on their senses. Thus, if a person has had prior knowledge of a dog that bites, then seeing a friendly dog may still be scary. This would also be more likely because the negative emotions tend to be in charge.

RBD (Active Dreams) at MCI diagnosis is related with a younger age, less AD, more parkinsonism, and a shorter survival. RBD was less common with LBD/AD females. A review of patients in a psychiatric hospital found symptoms indicative of RBD. Several reports found that home testing measures, including even a telephone interview for specific RBD symptoms might be as effective as formal overnight sleep test and much less of a hardship on the patient. Dopamine deficiency in patients with RBD was found to be a possible biomarker for dementia.

Parkinsonism at onset of MCI was always accompanied by RBD but did not predict DLB although it did increase any progression to DLB and was present 75% at time of death. It was associated with excessive daytime sleeping (EDS), less Alzheimer's and a shorter survival and progression to death.

Cognitive fluctuation biomarkers included telling time and EEGs: LBD-related cardiac (heart) nerve dysfunctions (an indicitative biomarker for DLB) were suggested to explain the differences in alertness. That is, when fluctuations in cardiac nerve function leads changes of oxygen to the brain with matching brain function fluctuations. These fluctuations continue to show up even late in the disease in 75% of patients.

Depression was identified as a serious, under-addressed problem with LBD, with some suggestions of its LBD related cause but few suggestions for treatment, other than increasing dopamine in some way.

Biomarkers were a big subject and covered a wide variety of objective, measurable tests. As care partners, we need to be especially aware of how valuable those obtained from the cerebral spinal fluid have become. There is a concerted effort to get people to submit to these tests, for their own needs but even more so for building up a network of subjects for clinical testing.

Drugs. There are still no drugs for treating DLB specifically, and no new ones for treating PDD. There are some variations of the old cholinesterase inhibitors (Aricept, Exelon and Razadyne) to make them longer-lasting, or used with a patch, or combined with drugs that reduce gastric side effects. There are a few drugs being tested.

• Pimavanserin, an anti-psychotic approved for use with PDD psychosis, is now being tested with other dementias.
• Neflamapimod, barely in Phase 2 testing for use with DLB, is believed to decrease brain inflammation that turns alpha-synuclien into Lewy bodies.
• (Zonisamide-(ZNS), first used to treat epilepsy, is in Phase 3 trials for treating parkinsonism in DLB with fewer side effects than anti-Parkinson's drugs. Drugs that get this far usually go to market but it could still be five years before we see it. (These trials can last up to 3 years and then, it still has to go through an approval process with the FDA that can last for 2 years.)
• Recruiting has begun for Phase 2 clinical trials of LY3154207, a PD drug that is hoped to increase dopamine function with fewer side effects.

Next week will be an overview of some of the subjects covered in the Patient and Care Partner track.

For more information about Lewy body disorders, read our books:
A Caregivers’ Guide to Lewy Body Dementia
Managing Cognitive Issues in Parkinson's and Lewy Body Dementia
Responsive Dementia Care: Fewer Behaviors Fewer Drugs
Riding A Roller Coaster with Lewy Body Dementia: A Manual for Staff

Helen and James Whitworth are not doctors, lawyers or social workers. As informed caregivers, they share the information here for educational purposes only. It should never be used instead of a professional's advice.