Disease-modifying therapeutic directions for Lewy-Body dementias

Frontiers in Neuroscience
Qiang ZhangNandakumar S Narayanan

Abstract

Dementia with Lewy bodies (DLB) is the second leading cause of dementia following Alzheimer's disease (AD) and accounts for up to 25% of all dementia. DLB is distinct from AD in that it involves extensive neuropsychiatric symptoms as well as motor symptoms, leads to enormous societal costs in terms of direct medical care and is associated with high financial and caregiver costs. Although, there are no disease-modifying therapies for DLB, we review several new therapeutic directions in treating DLB. We discuss progress in strategies to decrease the level of alpha-synuclein, to prevent the cell to cell transmission of misfolded alpha-synuclein, and the potential of brain stimulation in DLB.

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Citations

Dec 15, 2015·Maturitas·C Rodríguez-NogalesM J Blanco-Prieto
Oct 11, 2016·Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring·Meenakshi DauwanCornelis J Stam
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Apr 8, 2020·Robotic Surgery : Research and Reviews·Michel A AudetteJason E Blatt
Oct 4, 2021·Neuroscience Letters·Qiang ZhangNandakumar S Narayanan

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Methods Mentioned

BETA
transgenic

Related Concepts

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Alpha-Synuclein Aggregation (MDS)

Alpha-synucleins are small proteins that are believed to restrict the mobility of synpatic vesicles and inhibit neurotransmitter release. Aggregation of these proteins have been linked to several types of neurodegenerative diseases including dementia with Lewy bodies and Parkinson's disease. Here is the latest research on α-synuclein aggregation.

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