ArticleFrontiers in aging neuroscience2021
Parkinson's Disease Dementia: Synergistic Effects of Alpha-Synuclein, Tau, Beta-Amyloid, and Iron.
Article in Frontiers in aging neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- Nuclear dysfunction in aging and neurodegeneration.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Internal Heat Acupuncture Treatment Inhibits Ferroptosis in the Spinal Dorsal Horn in Neurotoxin-Induced Parkinson's Disease Rats.Applied biochemistry and biotechnology · 2026Article
- From Stress to Neurodegeneration: A New Look at the Pathogenesis of Parkinson's Disease.Biomedicines · 2026Review
- Iron dyshomeostasis in neuropsychiatric disorders.Frontiers in psychiatry · 2026Review
- Research Progress on Idebenone in Neurodegenerative Diseases.Aging medicine (Milton (N.S.W)) · 2025Review
- Role of iron in brain development, aging, and neurodegenerative diseases.Annals of medicine · 2025Review
- Converging pathologies in neurodegeneration: the mechanistic interplay between α-Synuclein and Tau in Alzheimer's and Parkinson's.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Review
- The association between blood urea nitrogen to albumin ratio and cognitive function in Parkinson's disease patients.Frontiers in neurology · 2025Article
- Cell-Free DNA, a Noninvasive Biomarker for Prediction and Detection of Neurodegenerative Diseases, New Insights, and Perspectives.CNS & neurological disorders drug targets · 2025Review
- MRI-derived brain iron, grey matter volume, and risk of dementia and Parkinson's disease: Observational and genetic analysis in the UK Biobank cohort.Neurobiology of disease · 2024Observational
- Rotenone Induces a Neuropathological Phenotype in Cholinergic-like Neurons Resembling Parkinson's Disease Dementia (PDD).Neurotoxicity research · 2024Article
- Tau accumulation is associated with dopamine deficiency in vivo in four-repeat tauopathies.European journal of nuclear medicine and molecular imaging · 2024Article
- Targeted Liposomal Co-Delivery Dopamine with 3-n-Butylphthalide for Effective Against Parkinson's Disease in Mice Model.International journal of nanomedicine · 2024Article
- Cognitive Impairment in Parkinson's Disease: An Updated Overview Focusing on Emerging Pharmaceutical Treatment Approaches.Medicina (Kaunas, Lithuania) · 2023Review
- Amyloid Fibrils ofInternational journal of molecular sciences · 2023Article
- The Roles of the Amyloid Beta Monomers in Physiological and Pathological Conditions.Biomedicines · 2023Review
- CHIR99021 Maintenance of the Cell Stemness by Regulating Cellular Iron Metabolism.Antioxidants (Basel, Switzerland) · 2023Article
- Quantitative Proteome and Transcriptome Dynamics Analysis Reveals Iron Deficiency Response Networks and Signature in Neuronal Cells.Molecules (Basel, Switzerland) · 2022Article
- Chronic Cerebral Hypoperfusion Aggravates Parkinson's Disease Dementia-Like Symptoms and Pathology in 6-OHDA-Lesioned Rat through Interfering with Sphingolipid Metabolism.Oxidative medicine and cellular longevity · 2022Article
- Liquid-Liquid Phase Separation Promotes Protein Aggregation and Its Implications in Ferroptosis in Parkinson's Disease Dementia.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease dementia (PDD) is a common complication of Parkinson's disease that seriously affects patients' health and quality of life. At present, the process and pathological mechanisms of PDD remain controversial, which hinders the development of treatments. An increasing number of clinical studies have shown that alpha-synuclein (α-syn), tau, beta-amyloid (Aβ), and iron are closely associated with PDD severity. Thus, we inferred the vicious cycle that causes oxidative stress (OS), due to the synergistic effects of α-syn, tau, Aβ, and, iron, and which plays a pivotal role in the mechanism underlying PDD. First, iron-mediated reactive oxygen species (ROS) production can lead to neuronal protein accumulation (e.g., α-syn andAβ) and cytotoxicity. In addition, regulation of post-translational modification of α-syn by iron affects the aggregation or oligomer formation of α-syn. Iron promotes tau aggregation and neurofibrillary tangles (NFTs) formation. High levels of iron, α-syn, Aβ, tau, and NFTs can cause severe OS and neuroinflammation, which lead to cell death. Then, the increasing formation of α-syn, Aβ, and NFTs further increase iron levels, which promotes the spread of α-syn and Aβ in the central and peripheral nervous systems. Finally, iron-induced neurotoxicity promotes the activation of glycogen synthase kinase 3β (GSK3β) related pathways in the synaptic terminals, which in turn play an important role in the pathological synergistic effects of α-syn, tau and Aβ. Thus, as the central factor regulating this vicious cycle, GSK3β is a potential target for the prevention and treatment of PDD; this is worthy of future study.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.