Abstract Body

Current pharmacological treatment of DLB is symptomatic and addresses each of he cardinal and supportive diagnostic features separately. Thus, treatment includes low doses of carbidopa/levodopa for parkinsonism; AChEIs for dementia; melatonin/low dose clonazepam for RBD; and low dose quetiapine/clozapine/pimavanserin for psychoses; SSRIs/bupropion for depression/anxiety; compression stocking/salt tablets/ fludrocortisone/midodrine for orthostatic hypotension; stool softeners/psyllium fiber supplements for constipation. Current management of MCI-LB is similar and symptom- driven. These and other treatments are variably effective and are better than nothing, but fall well short of the desired outcome of suppressing, reversing or even slowing progression of symptoms.

Future treatments will focus on identifying in life and then blunting the pathological processes that cause the disease in the first place. Pathological findings implicate widespread α-synuclein containing Lewy bodies; most cases also have excessive amounts of cortical Aβ neuritic plaques and tau containing neurofibrillary tangles. Our research has demonstrated that Aβ exacerbates cortical atrophy, hastens the accumulation of Lewy bodies and tangles and facilitates and speeds the rate of cognitive decline. A promising avenue of future treatment therefore is to lower the brain Aβ burden once it’s detected either by PET imaging or CSF/blood assays. According to this formulation, countering the toxic effects of excessive amyloid burden should be neuroprotective and moderate disease progression.