scholarly journals Alpha synuclein, the culprit in Parkinson disease, is required for normal immune function

Cell Reports ◽  
2022 ◽  
Vol 38 (2) ◽  
pp. 110090
Author(s):  
Md Masud Alam ◽  
De Yang ◽  
Xiao-Qing Li ◽  
Jia Liu ◽  
Timothy Carrel Back ◽  
...  
PEDIATRICS ◽  
1991 ◽  
Vol 88 (2) ◽  
pp. 359-363
Author(s):  
Jane D. Carver ◽  
Bernardo Pimentel ◽  
William I. Cox ◽  
Lewis A. Barness

Nucleotide (NT) nitrogen, a component of nonprotein nitrogen, accounts for approximately 0.1% to 0.15% of the total nitrogen content of human milk. The results of studies in animals indicate that dietary NTs may be required for maintenance of normal immune function. Thirty-seven healthy term infants were either breast-fed (n = 9) or fed SMA formula supplemented with 33 mg of NTs per liter (n = 13, NT+) or standard SMA formula (n = 15; NT-). At 2 months of age, natural killer cell percent cytotoxicity was significantly higher in the breast-fed and NT+ groups compared with the NT- group (41.7 ± 4.7, 32.2 ± 3.4, 21.7 ± 2.2%, respectively). Interleukin-2 production by stimulated mononuclear cells was higher in the NT+ compared with the NT- group at 2 months of age (0.90 ± 0.28 U/mL, 0.27 ± 0.11 U/mL, respectively); neither formula-fed group differed significantly from the breast-fed group. Rate of growth and incidence and severity of infections did not differ significantly among dietary groups. Nucleotides may be a component of human milk that contributes to the enhanced immunity of the breast-fed infant.


2021 ◽  
Author(s):  
Xiaobo Mao ◽  
Hao Gu ◽  
Donghoon Kim ◽  
Yasuyoshi Kimura ◽  
Ning Wang ◽  
...  

Pathologic alpha-synuclein (alpha-syn) spreads from cell-to-cell, in part, through binding to the lymphocyte-activation gene 3 (Lag3). Here we report that amyloid beta precursor-like protein 1 (Aplp1) forms a complex with Lag3 that facilitates the binding, internalization, transmission, and toxicity of pathologic alpha-syn. Deletion of both Aplp1 and Lag3 eliminates the loss of dopaminergic neurons and the accompanying behavioral deficits induced by alpha-syn preformed fibrils (PFF). Anti-Lag3 prevents the internalization of alpha-syn PFF by disrupting the interaction of Aplp1 and Lag3, and blocks the neurodegeneration induced by alpha-syn PFF in vivo. The identification of Aplp1 and the interplay with Lag3 for alpha-syn PFF induced pathology advances our understanding of the molecular mechanism of cell-to-cell transmission of pathologic alpha-syn and provides additional targets for therapeutic strategies aimed at preventing neurodegeneration in Parkinson disease and related alpha-synucleinopathies.


2018 ◽  
Vol 55 ◽  
pp. 15-17 ◽  
Author(s):  
Chaewon Shin ◽  
Sung-Hye Park ◽  
Ji Young Yun ◽  
Jung Hwan Shin ◽  
Han-Kwang Yang ◽  
...  

2007 ◽  
Vol 13 ◽  
pp. S125
Author(s):  
L. Brighina ◽  
N.K. Schneider ◽  
T.G. Lesnick ◽  
M. de Andrade ◽  
J.M. Cunningham ◽  
...  

PLoS Biology ◽  
2017 ◽  
Vol 15 (4) ◽  
pp. e1002601 ◽  
Author(s):  
Rita Machado de Oliveira ◽  
Hugo Vicente Miranda ◽  
Laetitia Francelle ◽  
Raquel Pinho ◽  
Éva M. Szegö ◽  
...  

2010 ◽  
Vol 28 (1) ◽  
pp. E7 ◽  
Author(s):  
Georgia Xiromerisiou ◽  
Efthimios Dardiotis ◽  
Vaïa Tsimourtou ◽  
Persa Maria Kountra ◽  
Konstantinos N. Paterakis ◽  
...  

Over the past few years, considerable progress has been made in understanding the molecular mechanisms of Parkinson disease (PD). Mutations in certain genes are found to cause monogenic forms of the disorder, with autosomal dominant or autosomal recessive inheritance. These genes include alpha-synuclein, parkin, PINK1, DJ-1, LRRK2, and ATP13A2. The monogenic variants are important tools in identifying cellular pathways that shed light on the pathogenesis of this disease. Certain common genetic variants are also likely to modulate the risk of PD. International collaborative studies and meta-analyses have identified common variants as genetic susceptibility risk/protective factors for sporadic PD.


2016 ◽  
Vol 263 (10) ◽  
pp. 1984-1992 ◽  
Author(s):  
Wei-Xi Xiong ◽  
Yi-Min Sun ◽  
Rong-Yuan Guan ◽  
Su-Shan Luo ◽  
Chen Chen ◽  
...  

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