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Title:
The interrelationship between intestinal immune cells and enteric α-synuclein in the progression of Parkinson’s disease | Neurological Sciences
Description:
Parkinson’s disease (PD) is a neurodegenerative disorder primarily characterized by motor impairment, resulting from the accumulation of α-synuclein and neuronal cell death in the substantia nigra of the midbrain. Emerging evidence suggests that α-synuclein aggregation may originate in the enteric nervous system (ENS) and subsequently propagate to the brain via the vagus nerve. Clinical observations, such as prodromal gastrointestinal dysfunction in PD patients and the increased incidence of PD among individuals with inflammatory bowel disease, support the hypothesis that abnormal intestinal inflammation may contribute to the onset of motor dysfunction and neuropathology in PD. This review examines recent findings on the interplay between intestinal immune cells and α-synuclein aggregation within the framework of gut-originated PD pathogenesis. It begins by discussing evidence linking dysbiosis and intestinal inflammation to α-synuclein aggregation in the ENS. Additionally, it explores the potential role of intestinal immune cells in influencing enteric neurons and α-synuclein aggregation, furthering the understanding of PD development.
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Keywords {🔍}
pubmed, disease, article, google, scholar, parkinsons, cas, central, intestinal, αsynuclein, bowel, gut, enteric, inflammatory, chen, patients, lin, disord, cells, cell, parkinson, alphasynuclein, gastrointestinal, wang, dis, liu, model, immune, system, brain, risk, med, mice, nervous, mov, zhang, inflammation, study, kim, lrrk, pathology, neurobiol, parkinsonism, lee, mol, dysfunction, increased, neurol, acta, neuropathol,
Topics {✒️}
month download article/chapter enteric phospho-alpha-synuclein aggregates central nervous system enteric alpha-synuclein expression hao-sen chiang accepted manuscript version enhances dectin-1–induced immunity anti-inflammatory cellular responses α-synuclein preformed fibrils intestinal neuro-immune axis activating tnf-alpha pathway short-chain fatty acids myeloid-derived suppressor cells enteric nervous system triggers age-related parkinson inflammatory bowel diseases α-synuclein mutant mice potential target-serum amyloid cd4 + th1/th2/t17 neutrophil extracellular traps maintain th17/treg balance human ipsc-based model intestinal epithelial barrier enteric α-synuclein pathological α-synuclein neuronal alpha-synuclein full article pdf gene expression profiles alpha-synuclein inclusions intestinal immune cells α-synuclein aggregation carlos javier madrid abnormal intestinal inflammation prodromal intestinal inflammation nigral dopaminergic system α-synuclein origin α-synuclein aggregates α-synuclein misfolding α-synuclein epitope gper1-mediated immunomodulation pathologic alpha-synuclein alpha-synuclein pathology privacy choices/manage cookies neuronal cell death published article forsyth cb wallen zd hill-yardin el disease-related brain pathology gut-originated pd pathogenesis
Questions {❓}
- Herrick MK, Tansey MG (2021) Is LRRK2 the missing link between inflammatory bowel disease and Parkinson’s disease?
- Shannon KM, Keshavarzian A, Dodiya HB, Jakate S, Kordower JH (2012) Is alpha-synuclein in the colon a biomarker for premotor Parkinson’s disease?
- Storelli E, Cassina N, Rasini E, Marino F, Cosentino M (2019) Do Th17 lymphocytes and IL-17 contribute to Parkinson’s disease?
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description:Parkinson’s disease (PD) is a neurodegenerative disorder primarily characterized by motor impairment, resulting from the accumulation of α-synuclein and neuronal cell death in the substantia nigra of the midbrain. Emerging evidence suggests that α-synuclein aggregation may originate in the enteric nervous system (ENS) and subsequently propagate to the brain via the vagus nerve. Clinical observations, such as prodromal gastrointestinal dysfunction in PD patients and the increased incidence of PD among individuals with inflammatory bowel disease, support the hypothesis that abnormal intestinal inflammation may contribute to the onset of motor dysfunction and neuropathology in PD. This review examines recent findings on the interplay between intestinal immune cells and α-synuclein aggregation within the framework of gut-originated PD pathogenesis. It begins by discussing evidence linking dysbiosis and intestinal inflammation to α-synuclein aggregation in the ENS. Additionally, it explores the potential role of intestinal immune cells in influencing enteric neurons and α-synuclein aggregation, furthering the understanding of PD development.
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Alpha-synuclein
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Parkinson’s disease
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description:Parkinson’s disease (PD) is a neurodegenerative disorder primarily characterized by motor impairment, resulting from the accumulation of α-synuclein and neuronal cell death in the substantia nigra of the midbrain. Emerging evidence suggests that α-synuclein aggregation may originate in the enteric nervous system (ENS) and subsequently propagate to the brain via the vagus nerve. Clinical observations, such as prodromal gastrointestinal dysfunction in PD patients and the increased incidence of PD among individuals with inflammatory bowel disease, support the hypothesis that abnormal intestinal inflammation may contribute to the onset of motor dysfunction and neuropathology in PD. This review examines recent findings on the interplay between intestinal immune cells and α-synuclein aggregation within the framework of gut-originated PD pathogenesis. It begins by discussing evidence linking dysbiosis and intestinal inflammation to α-synuclein aggregation in the ENS. Additionally, it explores the potential role of intestinal immune cells in influencing enteric neurons and α-synuclein aggregation, furthering the understanding of PD development.
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