Depression in dementia with Lewy bodies: a critical update

Jul 7, 2023Journal of neural transmission (Vienna, Austria : 1996)

Depression in Lewy Body Dementia: An Important Update

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Abstract

Depression affects an estimated 35% of individuals with dementia with Lewy bodies (DLB).

Depressive symptoms in DLB may occur throughout the clinical course and are often accompanied by apathy.
The frequency of depression is similar in DLB and Parkinson disease dementia, but its severity can be up to twice as high compared to Alzheimer disease.
Depression in DLB is frequently underdiagnosed and undertreated, which may be linked to various neurobiological mechanisms.
Dysfunctions in neurotransmitter systems, including monoaminergic, serotonergic, noradrenergic, and dopaminergic metabolism, may contribute to depression in DLB.
Effective treatments for pharmacotherapy-resistant cases may include modified electroconvulsive therapy, transcranial magnetic stimulation therapy, and deep brain stimulation.

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Depression with an estimated prevalence of 35% is a frequent manifestation of dementia with Lewy bodies (DLB), having negative effects on cognitive performance and life expectancy, yet the underlying neurobiology is poorly understood and most likely heterogeneous. Depressive symptoms in DLB can occur during the clinical course and, together with apathy, is a common prodromal neuropsychiatric symptom of this neurocognitive disorder in the group of Lewy body synucleinopathies. There are no essential differences in the frequency of depression in DLB and Parkinson disease-dementia (PDD), while its severity is up to twice as high as in Alzheimer disease (AD). Depression in DLB that is frequently underdiagnosed and undertreated, has been related to a variety of pathogenic mechanisms associated with the basic neurodegenerative process, in particular dysfunctions of neurotransmitter systems (decreased monoaminergic/serotonergic, noradrenergic and dopaminergic metabolism), α-synuclein pathology, synaptic zinc dysregulation, proteasome inhibition, gray matter volume loss in prefrontal and temporal areas as well as dysfunction of neuronal circuits with decreased functional connectivity of specific brain networks. Pharmacotherapy should avoid tricyclic antidepressants (anticholinergic adverse effects), second-generation antidepressants being a better choice, while modified electroconvulsive therapy, transcranial magnetic stimulation therapy and deep brain stimulation may be effective for pharmacotherapy-resistant cases. Since compared to depression in other dementias like Alzheimer disease and other parkinsonian syndromes, our knowledge of its molecular basis is limited, and further studies to elucidate the heterogeneous pathogenesis of depression in DLB are warranted.

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Depression in dementia with Lewy bodies: a critical update

Abstract

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