Linking To And Embedding “Distinguishing Prodromal Dementia with Lewy Bodies from Prodromal Alzheimer Disease” From Neurology Podcast With Links To The Original Article Article

Today, I review, link to, and embed “Distinguishing Prodromal Dementia with Lewy Bodies from Prodromal Alzheimer Disease” From Neurology Podcast With Links To The Original Article Article.*

*Differentiating Prodromal Dementia with Lewy Bodies from Prodromal Alzheimer’s Disease: A Pragmatic Review for Clinicians [PubMed Abstract] [Full-Text HTML] [Full-Text PDF]. Neurol Ther. 2024 Jun;13(3):885-906. doi: 10.1007/s40120-024-00620-x. Epub 2024 May 8.

And here is the abstract from the above article.

Abstract

This pragmatic review synthesises the current understanding of prodromal dementia with Lewy bodies (pDLB) and prodromal Alzheimer’s disease (pAD), including clinical presentations, neuropsychological profiles, neuropsychiatric symptoms, biomarkers, and indications for disease management. The core clinical features of dementia with Lewy bodies (DLB)-parkinsonism, complex visual hallucinations, cognitive fluctuations, and REM sleep behaviour disorder are common prodromal symptoms. Supportive clinical features of pDLB include severe neuroleptic sensitivity, as well as autonomic and neuropsychiatric symptoms. The neuropsychological profile in mild cognitive impairment attributable to Lewy body pathology (MCI-LB) tends to include impairment in visuospatial skills and executive functioning, distinguishing it from MCI due to AD, which typically presents with impairment in memory. pDLB may present with cognitive impairment, psychiatric symptoms, and/or recurrent episodes of delirium, indicating that it is not necessarily synonymous with MCI-LB. Imaging, fluid and other biomarkers may play a crucial role in differentiating pDLB from pAD. The current MCI-LB criteria recognise low dopamine transporter uptake using positron emission tomography or single photon emission computed tomography (SPECT), loss of REM atonia on polysomnography, and sympathetic cardiac denervation using meta-iodobenzylguanidine SPECT as indicative biomarkers with slowing of dominant frequency on EEG among others as supportive biomarkers. This review also highlights the emergence of fluid and skin-based biomarkers. There is little research evidence for the treatment of pDLB, but pharmacological and non-pharmacological treatments for DLB may be discussed with patients. Non-pharmacological interventions such as diet, exercise, and cognitive stimulation may provide benefit, while evaluation and management of contributing factors like medications and sleep disturbances are vital. There is a need to expand research across diverse patient populations to address existing disparities in clinical trial participation. In conclusion, an early and accurate diagnosis of pDLB or pAD presents an opportunity for tailored interventions, improved healthcare outcomes, and enhanced quality of life for patients and care partners.

Keywords: Biomarkers; Clinical diagnosis; Early-stage dementia; Mild cognitive impairment; Neuropsychological profile; Psychiatric symptoms; Treatment planning.

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Here is the embedding of the podcast:

Dec 5, 2024 Neurology Podcast

Dr. Vikram Karnik talks with Dr. Kate Wyman-Chick about distinguishing prodromal dementia with Lewy bodies from prodromal Alzheimer disease, the importance of early diagnosis, and the implications for clinical practice. Read the related article in Neurology: Clinical Practice. Disclosures can be found at Neurology.org.

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