Use the keywords feature with a free QxMD account.
Use Read by QxMD to access full text via your institution or open access sources.
Read also provides personalized recommendations to keep you up to date in your field.
Existing User
Sign InNew to Read
Sign Up#1
JOURNAL ARTICLE
Yeong Jin Kim, Bo-Ram Mun, Kyu Yeong Choi, Won-Seok Choi
The gut-brain axis (GBA) plays a significant role in various neurodegenerative disorders, such as Alzheimer's disease (AD), and the gut microbiome (GM) can bidirectionally communicate with the brain through the GBA. Thus, recent evidence indicates that the GM may affect the pathological features and the progression of AD in humans. The aim of our study was to elucidate the impact of probiotics on the pathological features of AD in a 5xFAD model. Probiotics ( Bifidobacterium lactis , Levilactobacillus brevis , and Limosilactobacillus fermentum ) were orally administered in 5xFAD mice to modify the GM composition...
February 23, 2024: Brain Sciences
#2
JOURNAL ARTICLE
Takashi Shimizu, Charles R Schutt, Yoshihiro Izumi, Noriyuki Tomiyasu, Zakaria Omahdi, Kuniyuki Kano, Hyota Takamatsu, Junken Aoki, Takeshi Bamba, Atsushi Kumanogoh, Masaki Takao, Sho Yamasaki
Gaucher disease (GD) is the most common lysosomal storage disease caused by recessive mutations in the degrading enzyme of β-glucosylceramide (β-GlcCer). However, it remains unclear how β-GlcCer causes severe neuronopathic symptoms, which are not fully treated by current therapies. We herein found that β-GlcCer accumulating in GD activated microglia through macrophage-inducible C-type lectin (Mincle) to induce phagocytosis of living neurons, which exacerbated Gaucher symptoms. This process was augmented by tumor necrosis factor (TNF) secreted from activated microglia that sensitized neurons for phagocytosis...
February 14, 2023: Immunity
#3
REVIEW
Qian-Kun Lv, Kang-Xin Tao, Xiao-Bo Wang, Xiao-Yu Yao, Meng-Zhu Pang, Jun-Yi Liu, Fen Wang, Chun-Feng Liu
BACKGROUND: Parkinson's disease (PD) is the second most common neurodegenerative disease, and is characterized by accumulation of α-synuclein (α-syn). Neuroinflammation driven by microglia is an important pathological manifestation of PD. α-Syn is a crucial marker of PD, and its accumulation leads to microglia M1-like phenotype polarization, activation of NLRP3 inflammasomes, and impaired autophagy and phagocytosis in microglia. Autophagy of microglia is related to degradation of α-syn and NLRP3 inflammasome blockage to relieve neuroinflammation...
January 4, 2023: Inflammation Research: Official Journal of the European Histamine Research Society ... [et Al.]
#4
REVIEW
Júlio César Claudino Dos Santos, Micael Porto Portela Lima, Gerly Anne de Castro Brito, Glauce Socorro de Barros Viana
The microbiota-gut-brain axis or simple gut-brain axis (GBA) is a complex and interactive bidirectional communication network linking the gut to the brain. Alterations in the composition of the gut microbiome have been linked to GBA dysfunction, central nervous system (CNS) inflammation, and dopaminergic degeneration, as those occurring in Parkinson's disease (PD). Besides inflammation, the activation of brain microglia is known to play a central role in the damage of dopaminergic neurons. Inflammation is attributed to the toxic effect of aggregated α-synuclein, in the brain of PD patients...
February 2023: Ageing Research Reviews
#5
JOURNAL ARTICLE
Chandra Sekhar Boddupalli, Shiny Nair, Glenn Belinsky, Joseph Gans, Erin Teeple, Tri-Hung Nguyen, Sameet Mehta, Lilu Guo, Martin L Kramer, Jiapeng Ruan, Honggge Wang, Matthew Davison, Dinesh Kumar, D J Vidyadhara, Bailin Zhang, Katherine Klinger, Pramod K Mistry
Background: Neuronopathic Gaucher disease (nGD) is a rare neurodegenerative disorder caused by biallelic mutations in GBA and buildup of glycosphingolipids in lysosomes. Neuronal injury and cell death are prominent pathological features; however, the role of GBA in individual cell types and involvement of microglia, blood-derived macrophages, and immune infiltrates in nGD pathophysiology remains enigmatic. Methods: Here, using single-cell resolution of mouse nGD brains, lipidomics, and newly generated biomarkers, we found induction of neuroinflammation pathways involving microglia, NK cells, astrocytes, and neurons...
August 16, 2022: ELife
#6
REVIEW
Miriam Højholt Terkelsen, Ida H Klaestrup, Victor Hvingelby, Johanne Lauritsen, Nicola Pavese, Marina Romero-Ramos
Multiple lines of clinical and pre-clinical research support a pathogenic role for neuroinflammation and peripheral immune system dysfunction in Parkinson's disease. In this paper, we have reviewed and summarised the published literature reporting evidence of neuroinflammation and peripheral immune changes in cohorts of patients with isolated REM sleep behaviour disorder and non-manifesting carriers of GBA or LRRK2 gene mutations, who have increased risk for Parkinsonism and synucleinopathies, and could be in the prodromal stage of these conditions...
2022: Journal of Parkinson's Disease
#7
JOURNAL ARTICLE
Li Chi, Xiao Cheng, Lishan Lin, Tao Yang, Jianbo Sun, Yiwei Feng, Fengyin Liang, Zhong Pei, Wei Teng
Background: Periodontal pathogen and gut microbiota are closely associated with the pathogenesis of Alzheimer's disease (AD). Porphyromonas gingivalis (Pg), the keystone periodontal pathogen, can induce cognitive impairment. The gut has a connection and communication with the brain, which is an important aspect of the gut-brain axis (GBA). In the present study, we investigate whether Pg induces cognitive impairment through disturbing the GBA. Methods: In this study, Pg was orally administered to mice, three times a week for 1 month...
2021: Frontiers in Cellular and Infection Microbiology
#8
JOURNAL ARTICLE
Electra Brunialti, Alessandro Villa, Marianna Mekhaeil, Federica Mornata, Elisabetta Vegeto, Adriana Maggi, Donato A Di Monte, Paolo Ciana
BACKGROUND: Homozygotic mutations in the GBA gene cause Gaucher's disease; moreover, both patients and heterozygotic carriers have been associated with 20- to 30-fold increased risk of developing Parkinson's disease. In homozygosis, these mutations impair the activity of β-glucocerebrosidase, the enzyme encoded by GBA, and generate a lysosomal disorder in macrophages, which changes morphology towards an engorged phenotype, considered the hallmark of Gaucher's disease. Notwithstanding the key role of macrophages in this disease, most of the effects in the brain have been attributed to the β-glucocerebrosidase deficit in neurons, while a microglial phenotype for these mutations has never been reported...
September 22, 2021: Journal of Neuroinflammation
#9
JOURNAL ARTICLE
Todd Logan, Matthew J Simon, Anil Rana, Gerald M Cherf, Ankita Srivastava, Sonnet S Davis, Ray Lieh Yoon Low, Chi-Lu Chiu, Meng Fang, Fen Huang, Akhil Bhalla, Ceyda Llapashtica, Rachel Prorok, Michelle E Pizzo, Meredith E K Calvert, Elizabeth W Sun, Jennifer Hsiao-Nakamoto, Yashas Rajendra, Katrina W Lexa, Devendra B Srivastava, Bettina van Lengerich, Junhua Wang, Yaneth Robles-Colmenares, Do Jin Kim, Joseph Duque, Melina Lenser, Timothy K Earr, Hoang Nguyen, Roni Chau, Buyankhishig Tsogtbaatar, Ritesh Ravi, Lukas L Skuja, Hilda Solanoy, Howard J Rosen, Bradley F Boeve, Adam L Boxer, Hilary W Heuer, Mark S Dennis, Mihalis S Kariolis, Kathryn M Monroe, Laralynne Przybyla, Pascal E Sanchez, Rene Meisner, Dolores Diaz, Kirk R Henne, Ryan J Watts, Anastasia G Henry, Kannan Gunasekaran, Giuseppe Astarita, Jung H Suh, Joseph W Lewcock, Sarah L DeVos, Gilbert Di Paolo
GRN mutations cause frontotemporal dementia (GRN-FTD) due to deficiency in progranulin (PGRN), a lysosomal and secreted protein with unclear function. Here, we found that Grn-/- mice exhibit a global deficiency in bis(monoacylglycero)phosphate (BMP), an endolysosomal phospholipid we identified as a pH-dependent PGRN interactor as well as a redox-sensitive enhancer of lysosomal proteolysis and lipolysis. Grn-/- brains also showed an age-dependent, secondary storage of glucocerebrosidase substrate glucosylsphingosine...
September 2, 2021: Cell
#10
REVIEW
Elena Coccia, Tim Ahfeldt
The derivation of human embryonic stem cells followed by the discovery of induced pluripotent stem cells and leaps in genome editing approaches have continuously fueled enthusiasm for the development of new models of neurodegenerative diseases such as Parkinson's disease (PD). PD is characterized by the relative selective loss of dopaminergic neurons (DNs) in specific areas of substantia nigra pars compacta (SNpc). While degeneration in late stages can be widespread, there is stereotypic early degeneration of these uniquely vulnerable neurons...
April 29, 2021: Stem Cell Research & Therapy
#11
REVIEW
Piplu Bhuiyan, Yinan Chen, Mazharul Karim, Hongquan Dong, Yanning Qian
Although the global incidence of neurodegenerative diseases has been steadily increasing, especially in adults, there are no effective therapeutic interventions. Neurodegeneration is a heterogeneous group of disorders that is characterized by the activation of immune cells in the central nervous system (CNS) (e.g., mast cells and microglia) and subsequent neuroinflammation. Mast cells are found in the brain and the gastrointestinal tract and play a role in "tuning" neuroimmune responses. The complex bidirectional communication between mast cells and gut microbiota coordinates various dynamic neuro-cellular responses, which propagates neuronal impulses from the gastrointestinal tract into the CNS...
July 2021: Brain Research Bulletin
#12
JOURNAL ARTICLE
Stephen Mullin, Morten Gersel Stokholm, Derralyn Hughes, Atul Mehta, Peter Parbo, Rainer Hinz, Nicola Pavese, David J Brooks, Anthony H V Schapira
BACKGROUND: Glucocerebrosidase gene mutations are a common genetic risk factor for Parkinson's disease. They exhibit incomplete penetrance. The objective of the present study was to measure microglial activation and dopamine integrity in glucocerebrosidase gene mutation carriers without Parkinson's disease compared to controls. METHODS: We performed PET scans on 9 glucocerebrosidase gene mutation carriers without Parkinson's disease and 29 age-matched controls. We measured microglial activation as 11 C-(R)-PK11195 binding potentials, and dopamine terminal integrity with 18 F-dopa influx constants...
March 2021: Movement Disorders: Official Journal of the Movement Disorder Society
#13
JOURNAL ARTICLE
Yael Pewzner-Jung, Tammar Joseph, Shani Blumenreich, Ayelet Vardi, Natalia Santos Ferreira, Soo Min Cho, Raya Eilam, Michael Tsoory, Inbal E Biton, Vlad Brumfeld, Rebecca Haffner-Krausz, Ori Brenner, Nir Sharabi, Yoseph Addadi, Tomer-Meir Salame, Ron Rotkopf, Noa Wigoda, Nadav Yayon, Alfred H Merrill, Raphael Schiffmann, Anthony H Futerman
Gaucher disease (GD) is currently the focus of considerable attention due primarily to the association between the gene that causes GD (GBA) and Parkinson's disease. Mouse models exist for the systemic (type 1) and for the acute neuronopathic forms (type 2) of GD. Here we report the generation of a mouse that phenotypically models chronic neuronopathic type 3 GD. Gba-/- ;Gbatg mice, which contain a Gba transgene regulated by doxycycline, accumulate moderate levels of the offending substrate in GD, glucosylceramide, and live for up to 10 months, i...
February 2021: Progress in Neurobiology
#14
JOURNAL ARTICLE
Ayelet Vardi, Shifra Ben-Dor, Soo Min Cho, Ulrich Kalinke, Julia Spanier, Anthony H Futerman
BACKGROUND: The type 1 interferon (IFN) response is part of the innate immune response and best known for its role in viral and bacterial infection. However, this pathway is also induced in sterile inflammation such as that which occurs in a number of neurodegenerative diseases, including neuronopathic Gaucher disease (nGD), a lysosomal storage disorder (LSD) caused by mutations in GBA. METHODS: Mice were injected with conduritol B-epoxide, an irreversible inhibitor of acid beta-glucosidase, the enzyme defective in nGD...
September 7, 2020: Journal of Neuroinflammation
#15
REVIEW
Bridget Martinez, Philip V Peplow
Parkinson's disease (PD) is the second most common age-related neurodegenerative disorder, with the clinical main symptoms caused by a loss of dopaminergic neurons in the substantia nigra, corpus striatum and brain cortex. Over 90% of patients with PD have sporadic PD and occur in people with no known family history of the disorder. Currently there is no cure for PD. Treatment with medications to increase dopamine relieves the symptoms but does not slow down or reverse the damage to neurons in the brain. Increasing evidence points to inflammation as a chief mediator of PD with inflammatory response mechanisms, involving microglia and leukocytes, activated following loss of dopaminergic neurons...
December 2017: Neural Regeneration Research
#16
JOURNAL ARTICLE
Einat B Vitner, Tamar Farfel-Becker, Natalia Santos Ferreira, Dena Leshkowitz, Piyush Sharma, Karl S Lang, Anthony H Futerman
BACKGROUND: Neuroinflammation is a key phenomenon in the pathogenesis of many neurodegenerative diseases. Understanding the mechanisms by which brain inflammation is engaged and delineating the key players in the immune response and their contribution to brain pathology is of great importance for the identification of novel therapeutic targets for these devastating diseases. Gaucher disease, the most common lysosomal storage disease, is caused by mutations in the GBA1 gene and is a significant risk factor for Parkinson's disease; in some forms of Gaucher disease, neuroinflammation is observed...
May 12, 2016: Journal of Neuroinflammation
#17
JOURNAL ARTICLE
Ida Berglin Enquist, Christophe Lo Bianco, Andreas Ooka, Eva Nilsson, Jan-Eric Månsson, Mats Ehinger, Johan Richter, Roscoe O Brady, Deniz Kirik, Stefan Karlsson
Gaucher disease (GD) is an autosomal recessive lysosomal storage disorder caused by mutations in the glucosidase, beta, acid (GBA) gene that encodes the lysosomal enzyme glucosylceramidase (GCase). GCase deficiency leads to characteristic visceral pathology and, in some patients, lethal neurological manifestations. Here, we report the generation of mouse models with the severe neuronopathic form of GD. To circumvent the lethal skin phenotype observed in several of the previous GCase-deficient animals, we genetically engineered a mouse model with strong reduction in GCase activity in all tissues except the skin...
October 30, 2007: Proceedings of the National Academy of Sciences of the United States of America
1
Make the most of Read.
Download the mobile app.
Download the mobile app.
Fetching more papers... 
