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Exosome dementia

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https://www.readbyqxmd.com/read/29775643/myocardial-infarction-induced-hippocampal-microtubule-damage-by-cardiac-originating-microrna-1-in-mice
#1
Lin-Lin Sun, Ming-Jing Duan, Ji-Chao Ma, Ling Xu, Meng Mao, Das Biddyut, Qin Wang, Chao Yang, Shuai Zhang, Yi Xu, Lin Yang, You Tian, Ying Liu, Sheng-Nan Xia, Ke-Xin Li, Zhuo Jin, Qiaojie Xiong, Jing Ai
Cardiovascular diseases are risk factors for dementia, but the mechanisms remain elusive. Here, we report that myocardial infarction (MI) generated by the ligation of the left coronary artery (LCA) could lead to increased miR-1 levels in the hippocampus and blood with neuronal microtubule damage and decreased TPPP/p25 protein expression in the hippocampus. These changes could be prevented by a knockdown of miR-1 using hippocampal stereotaxic injections of anti-miR-1 oligonucleotide fragments carried by a lentivirus vector (lenti-pre-AMO-miR-1)...
May 15, 2018: Journal of Molecular and Cellular Cardiology
https://www.readbyqxmd.com/read/29606187/the-serum-exosome-derived-microrna-135a-193b-and-384-were-potential-alzheimer-s-disease-biomarkers
#2
Ting Ting Yang, Chen Geng Liu, Shi Chao Gao, Yi Zhang, Pei Chang Wang
OBJECTIVE: MicroRNAs (miRs) are attractive molecules to be considered as one of the blood-based biomarkers for neurodegenerative disorders such as Alzheimer's disease (AD). The goal of this study was to explore their potential value as biomarkers for the diagnosis of AD. METHODS: The expression levels of exosomal miR-135a, -193b, and -384 in the serum from mild cognitive impairment (MCI), dementia of Alzheimer-type (DAT), Parkinson's disease with dementia (PDD), and vascular dementia (VaD) patients were measured with a real-time quantitative reverse transcriptase PCR (qRT-PCR) method...
February 2018: Biomedical and Environmental Sciences: BES
https://www.readbyqxmd.com/read/29559383/serum-exosomal-mir-223-serves-as-a-potential-diagnostic-and-prognostic-biomarker-for-dementia
#3
Hong Wei, Yuhao Xu, Wenlin Xu, Qianwen Zhou, Qi Chen, Meiling Yang, Fan Feng, Yueqin Liu, Xiaolan Zhu, Ming Yu, Yuefeng Li
The aims of this study were to examine the levels of serum and exosomal miR-137, miR-155 and miR-223, three neuroinflammation-related miRNAs, in dementia patients and to explore the value of these miRNAs for the diagnosis and prognostic evaluation of dementia. Thirty-two patients with dementia were enrolled, and sixteen volunteers without dementia served as controls. Serum exosomes were isolated by precipitation with ExoQuick and characterized by western blotting, nanoparticle-tracking analysis and immunofluorescence microscopy...
March 17, 2018: Neuroscience
https://www.readbyqxmd.com/read/29501530/neuronal-pentraxin-1-a-synaptic-derived-plasma-biomarker-in-alzheimer-s-disease
#4
Qiu-Lan Ma, Edmond Teng, Xiaohong Zuo, Mychica Jones, Bruce Teter, Evan Y Zhao, Cansheng Zhu, Tina Bilousova, Karen H Gylys, Liana G Apostolova, Mary Jo LaDu, Mir Ahamed Hossain, Sally A Frautschy, Gregory M Cole
Synaptic neurodegeneration is thought to be an early event initiated by soluble β-amyloid (Aβ) aggregates that closely correlates with cognitive decline in Alzheimer disease (AD). Apolipoprotein ε4 (APOE4) is the most common genetic risk factor for both familial AD (FAD) and sporadic AD; it accelerates Aβ aggregation and selectively impairs glutamate receptor function and synaptic plasticity. However, its molecular mechanisms remain elusive and these synaptic deficits are difficult to monitor. AD- and APOE4-dependent plasma biomarkers have been proposed, but synapse-related plasma biomarkers are lacking...
June 2018: Neurobiology of Disease
https://www.readbyqxmd.com/read/29434051/downregulation-of-exosomal-mir-204-5p-and-mir-632-as-a-biomarker-for-ftd-a-genfi-study
#5
Raphael Schneider, Paul McKeever, TaeHyung Kim, Caroline Graff, John Cornelis van Swieten, Anna Karydas, Adam Boxer, Howie Rosen, Bruce L Miller, Robert Laforce, Daniela Galimberti, Mario Masellis, Barbara Borroni, Zhaolei Zhang, Lorne Zinman, Jonathan Daniel Rohrer, Maria Carmela Tartaglia, Janice Robertson
OBJECTIVE: To determine whether exosomal microRNAs (miRNAs) in cerebrospinal fluid (CSF) of patients with frontotemporal dementia (FTD) can serve as diagnostic biomarkers, we assessed miRNA expression in the Genetic Frontotemporal Dementia Initiative (GENFI) cohort and in sporadic FTD. METHODS: GENFI participants were either carriers of a pathogenic mutation in progranulin, chromosome 9 open reading frame 72 or microtubule-associated protein tau or were at risk of carrying a mutation because a first-degree relative was a known symptomatic mutation carrier...
February 6, 2018: Journal of Neurology, Neurosurgery, and Psychiatry
https://www.readbyqxmd.com/read/29406582/high-complement-levels-in-astrocyte-derived-exosomes-of-alzheimer-disease
#6
Edward J Goetzl, Janice B Schwartz, Erin L Abner, Gregory A Jicha, Dimitrios Kapogiannis
OBJECTIVE: Astrocytes fulfill neuronal trophic roles normally, but are transformed in Alzheimer disease (AD) into A1-type reactive astrocytes that may destroy neurons through unknown mechanisms. METHODS: To investigate astrocyte inflammatory mechanisms, astrocyte-derived exosomes (ADEs) were isolated immunochemically from plasma samples of AD patients and matched controls for enzyme-linked immunosorbent assay quantification of complement proteins. RESULTS: ADE levels of C1q, C4b, C3d, factor B, factor D, Bb, C3b, and C5b-C9 terminal complement complex, but not mannose-binding lectin, normalized by the CD81 exosome marker were significantly higher for AD patients (n = 28) than age- and gender-matched controls (all p < 0...
March 2018: Annals of Neurology
https://www.readbyqxmd.com/read/29318971/-phenserine-and-inhibiting-pre-programmed-cell-death-in-pursuit-of-a-novel-intervention-for-alzheimer-s-disease
#7
Robert E Becker, Nigel H Greig, Debomoy K Lahiri, Joseph Bledsoe, Sarah Majercik, Clive Ballard, Dag Aarsland, Lon S Schneider, Douglas Flanagan, Ramprakash Govindarajan, Mary Sano, Luigi Ferrucci, Dimitrios Kapogiannis
BACKGROUND: Concussion (mild) and other moderate traumatic brain injury (TBI) and Alzheimer's disease (AD) share overlapping neuropathologies, including neuronal pre-programmed cell death (PPCD), and clinical impairments and disabilities. Multiple clinical trials targeting mechanisms based on the Amyloid Hypothesis of AD have so far failed, indicating that it is prudent for new drug developments to also pursue mechanisms independent of the Amyloid Hypothesis. To address these issue, we have proposed the use of an animal model of concussion/TBI as a supplement to AD transgenic mice to provide an indication of an AD drug candidate's potential for preventing PPCD and resulting progression towards dementia in AD...
January 10, 2018: Current Alzheimer Research
https://www.readbyqxmd.com/read/29198173/autophagy-inhibition-promotes-snca-alpha-synuclein-release-and-transfer-via-extracellular-vesicles-with-a-hybrid-autophagosome-exosome-like-phenotype
#8
Georgia Minakaki, Stefanie Menges, Agnes Kittel, Evangelia Emmanouilidou, Iris Schaeffner, Katalin Barkovits, Anna Bergmann, Edward Rockenstein, Anthony Adame, Franz Marxreiter, Brit Mollenhauer, Douglas Galasko, Edit Irén Buzás, Ursula Schlötzer-Schrehardt, Katrin Marcus, Wei Xiang, Dieter Chichung Lie, Kostas Vekrellis, Eliezer Masliah, Jürgen Winkler, Jochen Klucken
The autophagy-lysosome pathway (ALP) regulates intracellular homeostasis of the cytosolic protein SNCA/alpha-synuclein and is impaired in synucleinopathies, including Parkinson disease and dementia with Lewy bodies (DLB). Emerging evidence suggests that ALP influences SNCA release, but the underlying cellular mechanisms are not well understood. Several studies identified SNCA in exosome/extracellular vesicle (EV) fractions. EVs are generated in the multivesicular body compartment and either released upon its fusion with the plasma membrane, or cleared via the ALP...
2018: Autophagy
https://www.readbyqxmd.com/read/29163138/perspective-insights-into-disease-progression-diagnostics-and-therapeutic-approaches-in-alzheimer-s-disease-a-judicious-update
#9
REVIEW
Arif Tasleem Jan, Mudsser Azam, Safikur Rahman, Angham M S Almigeiti, Duk Hwan Choi, Eun Ju Lee, Qazi Mohd Rizwanul Haq, Inho Choi
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the progressive accumulation of β-amyloid fibrils and abnormal tau proteins in and outside of neurons. Representing a common form of dementia, aggravation of AD with age increases the morbidity rate among the elderly. Although, mutations in the ApoE4 act as potent risk factors for sporadic AD, familial AD arises through malfunctioning of APP, PSEN-1, and-2 genes. AD progresses through accumulation of amyloid plaques (Aβ) and neurofibrillary tangles (NFTs) in brain, which interfere with neuronal communication...
2017: Frontiers in Aging Neuroscience
https://www.readbyqxmd.com/read/29025866/declining-levels-of-functionally-specialized-synaptic-proteins-in-plasma-neuronal-exosomes-with-progression-of-alzheimer-s-disease
#10
Edward J Goetzl, Erin L Abner, Gregory A Jicha, Dimitrios Kapogiannis, Janice B Schwartz
Interactions of the presynaptic proteins, neuronal pentraxin 2 (NPTX2) and neurexin 2α (NRXN2α), with their respective postsynaptic functional partners, GluA4-containing glutamate (AMPA4) receptor and neuroligin 1 (NLGN1), enhance excitatory synaptic activity in some areas of the hippocampus and cerebral cortex. As early damage of such excitatory circuits in the brain tissues of participants with Alzheimer's disease (AD) correlates with cognitive losses, plasma neuron-derived exosome (NDE) levels of these 2 pairs of specialized synaptic proteins were quantified to assess their biomarker characteristics...
February 2018: FASEB Journal: Official Publication of the Federation of American Societies for Experimental Biology
https://www.readbyqxmd.com/read/28963439/neuroprotective-astrocyte-derived-insulin-insulin-like-growth-factor-1-stimulates-endocytic-processing-and-extracellular-release-of-neuron-bound-a%C3%AE-oligomers
#11
Jason Pitt, Kyle C Wilcox, Vanessa Tortelli, Luan Pereira Diniz, Maira S Oliveira, Cassandra Dobbins, Xiao-Wen Yu, Sathwik Nandamuri, Flávia C A Gomes, Nadia DiNunno, Kirsten L Viola, Fernanda G De Felice, Sergio T Ferreira, William L Klein
Synaptopathy underlying memory deficits in Alzheimer's disease (AD) is increasingly thought to be instigated by toxic oligomers of the amyloid beta peptide (AβOs). Given the long latency and incomplete penetrance of AD dementia with respect to Aβ pathology, we hypothesized that factors present in the CNS may physiologically protect neurons from the deleterious impact of AβOs. Here we employed physically separated neuron-astrocyte cocultures to investigate potential non-cell autonomous neuroprotective factors influencing AβO toxicity...
October 1, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28882786/exosomal-biomarkers-in-down-syndrome-and-alzheimer-s-disease
#12
REVIEW
Eric D Hamlett, Aurélie Ledreux, Huntington Potter, Heidi J Chial, David Patterson, Joaquin M Espinosa, Brianne M Bettcher, Ann-Charlotte Granholm
Every person with Down syndrome (DS) has the characteristic features of Alzheimer's disease (AD) neuropathology in their brain by the age of forty, and most go on to develop AD dementia. Since people with DS show highly variable levels of baseline function, it is often difficult to identify early signs of dementia in this population. The discovery of blood biomarkers predictive of dementia onset and/or progression in DS is critical for developing effective clinical diagnostics. Our recent studies show that neuron-derived exosomes, which are small extracellular vesicles secreted by most cells in the body, contain elevated levels of amyloid-beta peptides and phosphorylated-Tau that could indicate a preclinical AD phase in people with DS starting in childhood...
January 2018: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28794261/neuroprotective-astrocyte-derived-insulin-igf-1-stimulate-endocytic-processing-and-extracellular-release-of-neuron-bound-a%C3%AE-oligomers
#13
Jason Pitt, Kyle C Wilcox, Vanessa Tortelli, Luan Pereira Diniz, Maira S Oliveira, Cassandra Dobbins, Xiao-Wen Yu, Sathwik Nandamuri, Flávia C A Gomes, Nadia DiNunno, Kirsten L Viola, Fernanda G De Felice, Sergio T Ferreira, William L Klein
Synaptopathy underlying memory deficits in Alzheimer's disease (AD) is increasingly thought to be instigated by toxic oligomers of the amyloid beta peptide (AβOs). Given the long latency and incomplete penetrance of AD dementia with respect to Aβ pathology, we hypothesized that factors present in the CNS may physiologically protect neurons from the deleterious impact of AβOs. Here we employed physically-separated neuron-astrocyte co-cultures to investigate potential non cell-autonomous neuroprotective factors influencing AβO toxicity...
August 9, 2017: Molecular Biology of the Cell
https://www.readbyqxmd.com/read/28722658/the-golgi-localized-gamma-ear-containing-arf-binding-gga-protein-family-alters-alpha-synuclein-%C3%AE-syn-oligomerization-and-secretion
#14
Bjoern von Einem, Judith Eschbach, Martin Kiechle, Anke Wahler, Dietmar R Thal, Pamela J McLean, Jochen H Weishaupt, Albert C Ludolph, Christine A F von Arnim, Karin M Danzer
Several age-related neurodegenerative disorders are associated with protein misfolding and aggregation of toxic peptides. α-synuclein (α-syn) aggregation and the resulting cytotoxicity is a hallmark of Parkinson's disease (PD) as well as dementia with Lewy bodies. Rising evidence points to oligomeric and pre-fibrillar forms as the pathogenic species, and oligomer secretion seems to be crucial for the spreading and progression of PD pathology. Recent studies implicate that dysfunctions in endolysosomal/autophagosomal pathways increase α-syn secretion...
July 15, 2017: Aging
https://www.readbyqxmd.com/read/28684681/interplay-between-autophagy-exosomes-and-hiv-1-associated-neurological-disorders-new-insights-for-diagnosis-and-therapeutic-applications
#15
REVIEW
Chet Raj Ojha, Jessica Lapierre, Myosotys Rodriguez, Seth M Dever, Mohammad Asad Zadeh, Catherine DeMarino, Michelle L Pleet, Fatah Kashanchi, Nazira El-Hage
The autophagy-lysosomal pathway mediates a degradative process critical in the maintenance of cellular homeostasis as well as the preservation of proper organelle function by selective removal of damaged proteins and organelles. In some situations, cells remove unwanted or damaged proteins and RNAs through the release to the extracellular environment of exosomes. Since exosomes can be transferred from one cell to another, secretion of unwanted material to the extracellular environment in exosomes may have an impact, which can be beneficial or detrimental, in neighboring cells...
July 6, 2017: Viruses
https://www.readbyqxmd.com/read/28610892/novel-human-neuronal-tau-model-exhibiting-neurofibrillary-tangles-and-transcellular-propagation
#16
Patrick Reilly, Charisse N Winston, Kelsey R Baron, Margarita Trejo, Edward M Rockenstein, Johnny C Akers, Najla Kfoury, Marc Diamond, Eliezer Masliah, Robert A Rissman, Shauna H Yuan
Tauopathies are a class of neurodegenerative diseases, including Alzheimer's disease, frontotemporal dementia and progressive supranuclear palsy, which are associated with the pathological aggregation of tau protein into neurofibrillary tangles (NFT). Studies have characterized tau as a "prion-like" protein given its ability to form distinct, stable amyloid conformations capable of transcellular and multigenerational propagation in clonal fashion. It has been proposed that progression of tauopathy could be due to the prion-like propagation of tau, suggesting the possibility that end-stage pathologies, like NFT formation, may require an instigating event such as tau seeding...
October 2017: Neurobiology of Disease
https://www.readbyqxmd.com/read/28599681/brain-derived-exosomes-from-dementia-with-lewy-bodies-propagate-%C3%AE-synuclein-pathology
#17
Jennifer Ngolab, Ivy Trinh, Edward Rockenstein, Michael Mante, Jazmin Florio, Margarita Trejo, Deborah Masliah, Anthony Adame, Eliezer Masliah, Robert A Rissman
Proteins implicated in neurodegenerative conditions such as Alzheimer's disease (AD) and Dementia with Lewy Bodies (DLB) have been identified in bodily fluids encased in extracellular vesicles called exosomes. Whether exosomes found in DLB patients can transmit pathology is not clear. In this study, exosomes were successfully harvested through ultracentrifugation from brain tissue from DLB and AD patients as well as non-diseased brain tissue. Exosomes extracted from brains diagnosed with either AD or DLB contained aggregate-prone proteins...
June 9, 2017: Acta Neuropathologica Communications
https://www.readbyqxmd.com/read/28253991/micrornas-as-peripheral-biomarkers-in-aging-and-age-related-diseases
#18
REVIEW
S Kumar, M Vijayan, J S Bhatti, P H Reddy
MicroRNAs (miRNAs) are found in the circulatory biofluids considering the important molecules for biomarker study in aging and age-related diseases. Blood or blood components (serum/plasma) are primary sources of circulatory miRNAs and can release these in cell-free form either bound with some protein components or encapsulated with microvesicle particles, called exosomes. miRNAs are quite stable in the peripheral circulation and can be detected by high-throughput techniques like qRT-PCR, microarray, and sequencing...
2017: Progress in Molecular Biology and Translational Science
https://www.readbyqxmd.com/read/28241427/potential-modes-of-intercellular-%C3%AE-synuclein-transmission
#19
REVIEW
Dario Valdinocci, Rowan A W Radford, Sue Maye Siow, Roger S Chung, Dean L Pountney
Intracellular aggregates of the α-synuclein protein result in cell loss and dysfunction in Parkinson's disease and atypical Parkinsonism, such as multiple system atrophy and dementia with Lewy bodies. Each of these neurodegenerative conditions, known collectively as α-synucleinopathies, may be characterized by a different suite of molecular triggers that initiate pathogenesis. The mechanisms whereby α-synuclein aggregates mediate cytotoxicity also remain to be fully elucidated. However, recent studies have implicated the cell-to-cell spread of α-synuclein as the major mode of disease propagation between brain regions during disease progression...
February 22, 2017: International Journal of Molecular Sciences
https://www.readbyqxmd.com/read/28219659/dementia-like-pathology-in-type-2-diabetes-a-novel-microrna-mechanism
#20
Anuradha Kalani, Pankaj Chaturvedi, Claudio Maldonado, Philip Bauer, Irving G Joshua, Suresh C Tyagi, Neetu Tyagi
Although type-2 diabetes (T2D) has been reported to increase the risk of cognitive dysfunction and dementia, the underlying mechanisms remain unclear. Dementia-like pathology is attributed to the accumulation of cellular prion protein (PrPc ) which plays a role in cognitive dysfunction. However, its involvement and regulation in diabetic dementia-like pathology is not well understood. Using T2D db/db (leptin receptor knockout) mice subjected to object recognition and Y-maze behavioral tests, we determined that short-term memory was compromised and that the mice displayed abrupt spontaneous behaviour compared to db/m control mice...
April 2017: Molecular and Cellular Neurosciences
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