Dementia with Lewy bodies (DLB) is the second most common neurodegenerative dementia following Alzheimer disease. It stems from the formation of Lewy bodies, which contain aggregates of the misfolded protein, α-synuclein. These deposit in areas of the nervous system and brain, leading to neuronal cell death and causing clinically apparent symptoms. Because of its clinical overlap with other forms of dementia, DLB is often underdiagnosed and misdiagnosed. There is currently no cure for DLB and treatments are aimed at ameliorating specific symptoms.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.cger.2018.06.007 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Impact of Nutrition on the Gut Microbiota: Implications for Parkinson's Disease.
Nutr Rev
January 2025
Center for Neuroscience and Cell Biology (CNC), University of Coimbra, Coimbra 3004-504, Portugal.
Parkinson's disease (PD) is a multifactorial neurodegenerative disease that is characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta and by the anomalous accumulation of α-synuclein aggregates into Lewy bodies and Lewy neurites. Research suggests 2 distinct subtypes of PD: the brain-first subtype if the pathology arises from the brain and then spreads to the peripheral nervous system (PNS) and the body-first subtype, where the pathological process begins in the PNS and then spreads to the central nervous system. This review primarily focuses on the body-first subtype.
View Article and Find Full Text PDFAn audit on the assessment and management of osteoporosis in a Parkinson's and related diseases clinic in Australia.
J Neurol
January 2025
Macquarie Medical School, Parkinson's Disease Research Clinic, Macquarie University, Sydney, NSW, 2109, Australia.
Background: Patients with Parkinson's disease (PD) and atypical parkinsonian syndromes are at increased risk of falls and should be actively screened and treated for osteoporosis. In 2024, the Royal Australian College of General Practitioners (RACGP) revised their practice guidelines for diagnosing and managing osteoporosis in postmenopausal women and men aged over 50 years.
Objective: We conducted the first Australian study to audit these guidelines in patients with PD and atypical parkinsonian syndromes.
Unravelling the Role of Tyrosine and Tyrosine Hydroxylase in Parkinson's Disease: Exploring Nanoparticle-based Gene Therapies.
CNS Neurol Disord Drug Targets
January 2025
Department of Biotechnology, National Institute of Technology, Raipur, 492001, India.
Parkinson's disease (PD) is a neurodegenerative disorder that results from the progressive loss of neurons in the brain followed by symptoms such as slowness and rigidity in movement, sleep disorders, dementia and many more. The different mechanisms due to which the neuronal degeneration occurs have been discussed, such as mutation in PD related genes, formation of Lewy bodies, oxidation of dopamine. This review discusses current surgical treatment and gene therapies with novel developments proposed for PD.
View Article and Find Full Text PDFBrain-derived tau oligomer polymorphs: distinct aggregations, stability profiles, and biological activities.
Commun Biol
January 2025
Mitchell Center for Neurodegenerative Diseases, University of Texas Medical Branch, Galveston, TX, USA.
Aggregation of microtubule-associated tau protein is a distinct hallmark of several neurodegenerative disorders such as Alzheimer's disease (AD), dementia with Lewy bodies (DLB), and progressive supranuclear palsy (PSP). Tau oligomers are suggested to be the primary neurotoxic species that initiate aggregation and propagate prion-like structures. Furthermore, different diseases are shown to have distinct structural characteristics of aggregated tau, denoted as polymorphs.
View Article and Find Full Text PDFMotor cortical neuronal hyperexcitability associated with α-synuclein aggregation.
NPJ Parkinsons Dis
January 2025
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20852, USA.
ΑBSTRACT: In Parkinson's disease (PD), Lewy pathology deposits in the cerebral cortex, but how the pathology disrupts cortical circuit integrity and function remains poorly understood. To begin to address this question, we injected α-synuclein (αSyn) preformed fibrils (PFFs) into the dorsolateral striatum of mice to seed αSyn pathology in the cortical cortex and induce degeneration of midbrain dopaminergic neurons. We reported that αSyn aggregates accumulate in the motor cortex in a layer- and cell-subtype-specific pattern.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!