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BRAIN HEALTH
BRAIN HEALTH

Lewy Body Dementia: An update

By Gregory Michael Tomlinson, OMS-II, and Ramaswamy Sharma, MS, PhD

he United States Cost of Dementia Project, in its inaugural ism-like symptoms such as bradykinesia, shuffling gait and tremor. Sleep
statement, estimated an overall cost of $781 billion this year, disturbances are associated with LBD; rapid eye movement behavior
Twith the number of new dementia cases expected to double disorder (RBD), in which people act out their dreams, is more severe
over the next few decades as those born between 1946 to 1964 (the in patients with LBD. Depression may also occur. Since symptoms of
baby boom generation) cross 80 years of age and above. Dementia is an LBD overlap with other neurological disorders, it is difficult to diag-
umbrella term for a range of symptoms that includes loss of memory, nose. The diagnostic criteria for probable LBD include dementia with
problem-solving abilities and language difficulty, among others. Alz- progressive cognitive decline (tested using the Mini-Mental Status
heimer’s disease is the most common cause of dementia; Lewy body Exam) along with two additional features such as fluctuating cognition,
dementia (LBD), vascular dementia and frontotemporal dementia recurrent visual hallucinations, or spontaneous motor manifestations
are other primary causes of dementia. Approximately 20% to 30% of of Parkinsonism. Other “suggestive” features include RBD, neuroleptic
patients with dementia suffer from LBD. sensitivity, orthostatic hypertension, or imaging showing low dopamine
LBD has been further classified as dementia with Lewy bodies transporter activity in the basal ganglia.
(DLB) and Parkinson’s disease dementia (PDD) based on clinical cri- LBD is characterized by the presence of Lewy bodies and Lewy
teria. In DLB, dementia precedes or occurs within a year of disorders of neurites, abnormal cytoplasmic aggregates consisting primarily of
movement. In PDD, a patient diagnosed with Parkinson’s disease (PD) misfolded alpha-synuclein and ubiquitin, which disrupt neuronal
begins to develop dementia symptoms a year or more after the original function and trigger cell death. Alpha-synuclein is expressed
diagnosis. However, since many clinical features of Parkinson’s disease primarily in the brain, mostly within neuronal presynaptic axon
and DLB are similar, new classification systems are being proposed to terminals, wherein it attenuates neurotransmitter release. In LBD,
appropriately diagnose and identify patients for new clinical trials. alpha-synuclein forms aggregates of insoluble fibrils that impair the
Symptoms vary from patient to patient and with time; these include function of microtubules, mitochondria, proteasomes and lysosomes,
progressive dementia with or without memory loss, unpredictable fluc- and interferes with calcium signaling and synapses, resulting in
tuation in cognition, visual hallucinations, delusions and Parkinson- acetylcholine deficiency and, consequently, visual hallucinations.

18 SAN ANTONIO MEDICINE • June 2025