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Exosome dementia

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https://www.readbyqxmd.com/read/27755974/neuronal-exosomes-reveal-alzheimer-s-disease-biomarkers-in-down-syndrome
#1
Eric D Hamlett, Edward J Goetzl, Aurélie Ledreux, Vitaly Vasilevko, Heather A Boger, Angela LaRosa, David Clark, Steven L Carroll, María Carmona-Iragui, Juan Fortea, Elliott J Mufson, Marwan Sabbagh, Abdul H Mohammed, Dean Hartley, Eric Doran, Ira T Lott, Ann-Charlotte Granholm
INTRODUCTION: Individuals with Down syndrome (DS) exhibit Alzheimer's disease (AD) neuropathology and dementia early in life. Blood biomarkers of AD neuropathology would be valuable, as non-AD intellectual disabilities of DS and AD dementia overlap clinically. We hypothesized that elevations of amyloid-β (Aβ) peptides and phosphorylated-tau in neuronal exosomes may document preclinical AD. METHODS: AD neuropathogenic proteins Aβ1-42, P-T181-tau, and P-S396-tau were quantified by enzyme-linked immunosorbent assays in extracts of neuronal exosomes purified from blood of individuals with DS and age-matched controls...
October 15, 2016: Alzheimer's & Dementia: the Journal of the Alzheimer's Association
https://www.readbyqxmd.com/read/27732842/cell-to-cell-transmission-of-dipeptide-repeat-proteins-linked-to-c9orf72-als-ftd
#2
Thomas Westergard, Brigid K Jensen, Xinmei Wen, Jingli Cai, Elizabeth Kropf, Lorraine Iacovitti, Piera Pasinelli, Davide Trotti
Aberrant hexanucleotide repeat expansions in C9orf72 are the most common genetic change underlying amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). RNA transcripts containing these expansions undergo repeat-associated non-ATG translation (RAN-T) to form five dipeptide repeat proteins (DPRs). DPRs are found as aggregates throughout the CNS of C9orf72-ALS/FTD patients, and some cause degeneration when expressed in vitro in neuronal cultures and in vivo in animal models. The spread of characteristic disease-related proteins drives the progression of pathology in many neurodegenerative diseases...
October 11, 2016: Cell Reports
https://www.readbyqxmd.com/read/27601437/decreased-synaptic-proteins-in-neuronal-exosomes-of-frontotemporal-dementia-and-alzheimer-s-disease
#3
Edward J Goetzl, Dimitrios Kapogiannis, Janice B Schwartz, Iryna V Lobach, Laura Goetzl, Erin L Abner, Gregory A Jicha, Anna M Karydas, Adam Boxer, Bruce L Miller
Synaptic dysfunction occurs early in senile dementias, presumably as a result of decreased levels of functional synaptic proteins as found in autopsied brains of patients with Alzheimer's disease (AD) or frontotemporal dementia (FTD). Plasma neuronal-derived exosomes (NDEs) were recovered by precipitation and immunoabsorption from 12 patients with AD, 16 with FTD, and 28 controls in a cross-sectional study, and from 9 patients with AD, 10 with FTD, and 19 controls in a longitudinal study. Six synaptic proteins in NDE extracts were quantified by ELISAs and normalized for exosome amounts...
December 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27511944/cargo-proteins-of-plasma-astrocyte-derived-exosomes-in-alzheimer-s-disease
#4
Edward J Goetzl, Maja Mustapic, Dimitrios Kapogiannis, Erez Eitan, Irina V Lobach, Laura Goetzl, Janice B Schwartz, Bruce L Miller
Efficient intercellular transfer of RNAs, proteins, and lipids as protected exosomal cargo has been demonstrated in the CNS, but distinct physiologic and pathologic roles have not been well defined for this pathway. The capacity to isolate immunochemically human plasma neuron-derived exosomes (NDEs), containing neuron-specific cargo, has permitted characterization of CNS-derived exosomes in living humans. Constituents of the amyloid β-peptide (Aβ)42-generating system now are examined in 2 distinct sets of human neural cells by quantification in astrocyte-derived exosomes (ADEs) and NDEs, enriched separately from plasmas of patients with Alzheimer's disease (AD) or frontotemporal dementia (FTD) and matched cognitively normal controls...
November 2016: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/27460707/proteomic-analysis-of-fus-interacting-proteins-provides-insights-into-fus-function-and-its-role-in-als
#5
Marisa Kamelgarn, Jing Chen, Lisha Kuang, Alexandra Arenas, Jianjun Zhai, Haining Zhu, Jozsef Gal
Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease. Mutations in the Fused in Sarcoma/Translocated in Liposarcoma (FUS/TLS) gene cause a subset of familial ALS cases and are also implicated in sporadic ALS. FUS is typically localized to the nucleus. The ALS-related FUS mutations cause cytoplasmic mis-localization and the formation of stress granule-like structures. Abnormal cytoplasmic FUS localization was also found in a subset of frontotemporal dementia (FTLD) cases without FUS mutations...
October 2016: Biochimica et Biophysica Acta
https://www.readbyqxmd.com/read/27408937/prediction-of-conversion-from-mild-cognitive-impairment-to-dementia-with-neuronally-derived-blood-exosome-protein-profile
#6
Charisse N Winston, Edward J Goetzl, Johnny C Akers, Bob S Carter, Edward M Rockenstein, Douglas Galasko, Eliezer Masliah, Robert A Rissman
INTRODUCTION: Levels of Alzheimer's disease (AD)-related proteins in plasma neuronal derived exosomes (NDEs) were quantified to identify biomarkers for prediction and staging of mild cognitive impairment (MCI) and AD. METHODS: Plasma exosomes were extracted, precipitated, and enriched for neuronal source by anti-L1CAM antibody absorption. NDEs were characterized by size (Nanosight) and shape (TEM) and extracted NDE protein biomarkers were quantified by ELISAs. Plasma NDE cargo was injected into normal mice, and results were characterized by immunohistochemistry to determine pathogenic potential...
2016: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
https://www.readbyqxmd.com/read/27102354/bone-marrow-derived-mesenchymal-stem-cells-improve-diabetes-induced-cognitive-impairment-by-exosome-transfer-into-damaged-neurons-and-astrocytes
#7
Masako Nakano, Kanna Nagaishi, Naoto Konari, Yuki Saito, Takako Chikenji, Yuka Mizue, Mineko Fujimiya
The incidence of dementia is higher in diabetic patients, but no effective treatment has been developed. This study showed that rat bone marrow mesenchymal stem cells (BM-MSCs) can improve the cognitive impairments of STZ-diabetic mice by repairing damaged neurons and astrocytes. The Morris water maze test demonstrated that cognitive impairments induced by diabetes were significantly improved by intravenous injection of BM-MSCs. In the CA1 region of the hippocampus, degeneration of neurons and astrocytes, as well as synaptic loss, were prominent in diabetes, and BM-MSC treatment successfully normalized them...
2016: Scientific Reports
https://www.readbyqxmd.com/read/26974972/enabling-metabolomics-based-biomarker-discovery-studies-using-molecular-phenotyping-of-exosome-like-vesicles
#8
Tatiana Altadill, Irene Campoy, Lucia Lanau, Kirandeep Gill, Marina Rigau, Antonio Gil-Moreno, Jaume Reventos, Stephen Byers, Eva Colas, Amrita K Cheema
Identification of sensitive and specific biomarkers with clinical and translational utility will require smart experimental strategies that would augment expanding the breadth and depth of molecular measurements within the constraints of currently available technologies. Exosomes represent an information rich matrix to discern novel disease mechanisms that are thought to contribute to pathologies such as dementia and cancer. Although proteomics and transcriptomic studies have been reported using Exosomes-Like Vesicles (ELVs) from different sources, exosomal metabolome characterization and its modulation in health and disease remains to be elucidated...
2016: PloS One
https://www.readbyqxmd.com/read/26973102/loss-of-exosomes-in-progranulin-associated-frontotemporal-dementia
#9
Luisa Benussi, Miriam Ciani, Elisa Tonoli, Michela Morbin, Luisa Palamara, Diego Albani, Federica Fusco, Gianluigi Forloni, Michela Glionna, Monika Baco, Anna Paterlini, Silvia Fostinelli, Benedetta Santini, Elisabetta Galbiati, Paola Gagni, Marina Cretich, Giuliano Binetti, Fabrizio Tagliavini, Davide Prosperi, Marcella Chiari, Roberta Ghidoni
Many cells of the nervous system have been shown to release exosomes, a subclass of secreted vesicles of endosomal origin capable of transferring biomolecules among cells: this transfer modality represents a novel physiological form of intercellular communication between neural cells. Herein, we demonstrated that progranulin (PGRN), a protein targeted to the classical secretory pathway, is also secreted in association with exosomes by human primary fibroblasts. Moreover, we demonstrated that null mutations in the progranulin gene (GRN), a major cause of frontotemporal dementia, strongly reduce the number of released exosomes and alter their composition...
April 2016: Neurobiology of Aging
https://www.readbyqxmd.com/read/26647156/induction-of-%C3%AE-synuclein-aggregate-formation-by-csf-exosomes-from-patients-with-parkinson-s-disease-and-dementia-with-lewy-bodies
#10
Anne Stuendl, Marcel Kunadt, Niels Kruse, Claudia Bartels, Wiebke Moebius, Karin M Danzer, Brit Mollenhauer, Anja Schneider
Extracellular α-synuclein has been proposed as a crucial mechanism for induction of pathological aggregate formation in previously healthy cells. In vitro, extracellular α-synuclein is partially associated with exosomal vesicles. Recently, we have provided evidence that exosomal α-synuclein is present in the central nervous system in vivo. We hypothesized that exosomal α-synuclein species from patients with α-synuclein related neurodegeneration serve as carriers for interneuronal disease transmission. We isolated exosomes from cerebrospinal fluid from patients with Parkinson's disease, dementia with Lewy bodies, progressive supranuclear palsy as a non-α-synuclein related disorder that clinically overlaps with Parkinson's disease, and neurological controls...
February 2016: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/26426747/plasma-exosomal-mirnas-in-persons-with-and-without-alzheimer-disease-altered-expression-and-prospects-for-biomarkers
#11
COMPARATIVE STUDY
Giovanni Lugli, Aaron M Cohen, David A Bennett, Raj C Shah, Christopher J Fields, Alvaro G Hernandez, Neil R Smalheiser
To assess the value of exosomal miRNAs as biomarkers for Alzheimer disease (AD), the expression of microRNAs was measured in a plasma fraction enriched in exosomes by differential centrifugation, using Illumina deep sequencing. Samples from 35 persons with a clinical diagnosis of AD dementia were compared to 35 age and sex matched controls. Although these samples contained less than 0.1 microgram of total RNA, deep sequencing gave reliable and informative results. Twenty miRNAs showed significant differences in the AD group in initial screening (miR-23b-3p, miR-24-3p, miR-29b-3p, miR-125b-5p, miR-138-5p, miR-139-5p, miR-141-3p, miR-150-5p, miR-152-3p, miR-185-5p, miR-338-3p, miR-342-3p, miR-342-5p, miR-548at-5p, miR-659-5p, miR-3065-5p, miR-3613-3p, miR-3916, miR-4772-3p, miR-5001-3p), many of which satisfied additional biological and statistical criteria, and among which a panel of seven miRNAs were highly informative in a machine learning model for predicting AD status of individual samples with 83-89% accuracy...
2015: PloS One
https://www.readbyqxmd.com/read/26407718/nef-exosomes-isolated-from-the-plasma-of-individuals-with-hiv-associated-dementia-had-can-induce-a%C3%AE-1-42-secretion-in-sh-sy5y-neural-cells
#12
Mahfuz B Khan, Michelle J Lang, Ming-Bo Huang, Andrea Raymond, Vincent C Bond, Bruce Shiramizu, Michael D Powell
In the era of combined antiretroviral therapy (CART), many of the complications due to HIV-1 infection have diminished. One exception is HIV-associated neurocognitive disorder (HAND). HAND is a spectrum of disorders in cognitive function that ranges from asymptomatic disease to severe dementia (HAD). The milder form of HAND has actually remained the same or slightly increased in prevalence in the CART era. Even in individuals who have maintained undetectable HIV RNA loads, viral proteins such as Nef and Tat can continue to be expressed...
April 2016: Journal of Neurovirology
https://www.readbyqxmd.com/read/26373282/frontotemporal-dementia-associated-n279k-tau-mutant-disrupts-subcellular-vesicle-trafficking-and-induces-cellular-stress-in-ipsc-derived-neural-stem-cells
#13
Melissa C Wren, Jing Zhao, Chia-Chen Liu, Melissa E Murray, Yuka Atagi, Mary D Davis, Yuan Fu, Hirotaka J Okano, Kotaro Ogaki, Audrey J Strongosky, Pawel Tacik, Rosa Rademakers, Owen A Ross, Dennis W Dickson, Zbigniew K Wszolek, Takahisa Kanekiyo, Guojun Bu
BACKGROUND: Pallido-ponto-nigral degeneration (PPND), a major subtype of frontotemporal dementia with parkinsonism related to chromosome 17 (FTDP-17), is a progressive and terminal neurodegenerative disease caused by c.837 T > G mutation in the MAPT gene encoding microtubule-associated protein tau (rs63750756; N279K). This MAPT mutation induces alternative splicing of exon 10, resulting in a modification of microtubule-binding region of tau. Although mutations in the MAPT gene have been linked to multiple tauopathies including Alzheimer's disease, frontotemporal dementia and progressive supranuclear palsy, knowledge regarding how tau N279K mutation causes PPND/FTDP-17 is limited...
September 15, 2015: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/26273689/low-neural-exosomal-levels-of-cellular-survival-factors-in-alzheimer-s-disease
#14
Edward J Goetzl, Adam Boxer, Janice B Schwartz, Erin L Abner, Ronald C Petersen, Bruce L Miller, Olga D Carlson, Maja Mustapic, Dimitrios Kapogiannis
Transcription factors that mediate neuronal defenses against diverse stresses were quantified in plasma neural-derived exosomes of Alzheimer's disease or frontotemporal dementia patients and matched controls. Exosomal levels of low-density lipoprotein receptor-related protein 6, heat-shock factor-1, and repressor element 1-silencing transcription factor all were significantly lower in Alzheimer's disease patients than controls (P < 0.0001). In frontotemporal dementia, the only significant difference was higher levels of repressor element 1-silencing transcription factor than in controls...
July 2015: Annals of Clinical and Translational Neurology
https://www.readbyqxmd.com/read/26172304/exposure-to-als-ftd-csf-generates-tdp-43-aggregates-in-glioblastoma-cells-through-exosomes-and-tnts-like-structure
#15
Xuebing Ding, Mingming Ma, Junfang Teng, Robert K F Teng, Shuang Zhou, Jingzheng Yin, Ekokobe Fonkem, Jason H Huang, Erxi Wu, Xuejing Wang
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) represent a continuum of devastating neurodegenerative diseases, characterized by transactive response DNA-binding protein of 43 kDa (TDP-43) aggregates accumulation throughout the nervous system. Despite rapidly emerging evidence suggesting the hypothesis of 'prion-like propagation' of TDP-43 positive inclusion in the regional spread of ALS symptoms, whether and how TDP-43 aggregates spread between cells is not clear. Herein, we established a cerebrospinal fluid (CSF)-cultured cell model to dissect mechanisms governing TDP-43 aggregates formation and propagation...
September 15, 2015: Oncotarget
https://www.readbyqxmd.com/read/26062630/altered-lysosomal-proteins-in-neural-derived-plasma-exosomes-in-preclinical-alzheimer-disease
#16
Edward J Goetzl, Adam Boxer, Janice B Schwartz, Erin L Abner, Ronald C Petersen, Bruce L Miller, Dimitrios Kapogiannis
OBJECTIVE: Diverse autolysosomal proteins were quantified in neurally derived blood exosomes from patients with Alzheimer disease (AD) and controls to investigate disordered neuronal autophagy. METHODS: Blood exosomes obtained once from patients with AD (n = 26) or frontotemporal dementia (n = 16), other patients with AD (n = 20) both when cognitively normal and 1 to 10 years later when diagnosed, and case controls were enriched for neural sources by anti-human L1CAM antibody immunoabsorption...
July 7, 2015: Neurology
https://www.readbyqxmd.com/read/25484190/autophagy-modulates-snca-%C3%AE-synuclein-release-thereby-generating-a-hostile-microenvironment
#17
Anne-Maria Poehler, Wei Xiang, Philipp Spitzer, Verena Elisabeth Luise May, Holger Meixner, Edward Rockenstein, Oldriska Chutna, Tiago Fleming Outeiro, Juergen Winkler, Eliezer Masliah, Jochen Klucken
SNCA/α-synuclein aggregation plays a crucial role in synucleinopathies such as Parkinson disease and dementia with Lewy bodies. Aggregating and nonaggregating SNCA species are degraded by the autophagy-lysosomal pathway (ALP). Previously, we have shown that the ALP is not only responsible for SNCA degradation but is also involved in the intracellular aggregation process of SNCA. An additional role of extracellular SNCA in the pathology of synucleinopathies substantiating a prion-like propagation hypothesis has been suggested since released SNCA species and spreading of SNCA pathology throughout neural cells have been observed...
2014: Autophagy
https://www.readbyqxmd.com/read/25342129/dysfunctionally-phosphorylated-type-1-insulin-receptor-substrate-in-neural-derived-blood-exosomes-of-preclinical-alzheimer-s-disease
#18
Dimitrios Kapogiannis, Adam Boxer, Janice B Schwartz, Erin L Abner, Arya Biragyn, Umesh Masharani, Lynda Frassetto, Ronald C Petersen, Bruce L Miller, Edward J Goetzl
Insulin resistance causes diminished glucose uptake in similar regions of the brain in Alzheimer's disease (AD) and type 2 diabetes mellitus (DM2). Brain tissue studies suggested that insulin resistance is caused by low insulin receptor signaling attributable to its abnormal association with more phospho (P)-serine-type 1 insulin receptor substrate (IRS-1) and less P-tyrosine-IRS-1. Plasma exosomes enriched for neural sources by immunoabsorption were obtained once from 26 patients with AD, 20 patients with DM2, 16 patients with frontotemporal dementia (FTD), and matched case control subjects...
February 2015: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/25130657/identification-of-preclinical-alzheimer-s-disease-by-a-profile-of-pathogenic-proteins-in-neurally-derived-blood-exosomes-a-case-control-study
#19
MULTICENTER STUDY
Massimo S Fiandaca, Dimitrios Kapogiannis, Mark Mapstone, Adam Boxer, Erez Eitan, Janice B Schwartz, Erin L Abner, Ronald C Petersen, Howard J Federoff, Bruce L Miller, Edward J Goetzl
BACKGROUND: Proteins pathogenic in Alzheimer's disease (AD) were extracted from neurally derived blood exosomes and quantified to develop biomarkers for the staging of sporadic AD. METHODS: Blood exosomes obtained at one time-point from patients with AD (n = 57) or frontotemporal dementia (FTD) (n = 16), and at two time-points from others (n = 24) when cognitively normal and 1 to 10 years later when diagnosed with AD were enriched for neural sources by immunoabsorption...
June 2015: Alzheimer's & Dementia: the Journal of the Alzheimer's Association
https://www.readbyqxmd.com/read/25119742/microrna-193b-is-a-regulator-of-amyloid-precursor-protein-in-the-blood-and-cerebrospinal-fluid-derived-exosomal-microrna-193b-is-a-biomarker-of-alzheimer-s-disease
#20
Chen-Geng Liu, Jing Song, Yue-Qi Zhang, Pei-Chang Wang
Amyloid precursor protein (APP) has an important function in the generation of Alzheimer's disease (AD). In our previous study, miR‑193b was found to be downregulated in the hippocampi of 9‑month‑old APP/PS1 double‑transgenic mice using microRNA (miR) array. In the present study, bioinformatic analyses showed that miR‑193b was a miR that was predicted to potentially target the 3'‑untranslated region (UTR) of APP. Subsequently, the function of miR‑193b on APP was studied. The levels of miR‑193b, exosomal miR‑193b, Aβ, tau, p‑tau, HCY and APOE in samples from APP/PS1 double‑transgenic mice, mild cognitive impairment (MCI) and dementia of Alzheimer‑type (DAT) patients, were measured...
November 2014: Molecular Medicine Reports
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