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https://www.readbyqxmd.com/read/29305855/microglia-derived-extracellular-vesicles-in-alzheimer-s-disease-a-double-edged-sword
#1
REVIEW
Teresa Trotta, Maria Antonietta Panaro, Antonia Cianciulli, Giorgio Mori, Adriana Di Benedetto, Chiara Porro
Extracellular vesicles (EVs), based on their origin or size, can be classified as apoptotic bodies, microvesicles (MVs)/microparticles (MPs), and exosomes. EVs are one of the new emerging modes of communication between cells that are providing new insights into the pathophysiology of several diseases. EVs released from activated or apoptotic cells contain specific proteins (signaling molecules, receptors, integrins, cytokines), bioactive lipids, nucleic acids (mRNA, miRNA, small non coding RNAs, DNA) from their progenitor cells...
January 3, 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29305061/a-refined-concept-alpha-synuclein-dysregulation-disease
#2
REVIEW
Hideki Mochizuki, Chi-Jing Choong, Eliezer Masliah
Alpha synuclein (αSyn) still remains a mysterious protein even two decades after SNCA encoding it was identified as the first causative gene of familial Parkinson's disease (PD). Accumulation of αSyn causes α-synucleinopathies including PD, dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Recent advances in therapeutic approaches offer new antibody-, vaccine-, antisense-oligonucleotide- and small molecule-based options to reduce αSyn protein levels and aggregates in patient's brain. Gathering research information of other neurological disease particularly Alzheimer's disease, recent disappointment of an experimental amyloid plaques busting antibody in clinical trials underscores the difficulty of treating people who show even mild dementia as damage in their brain may already be too extensive...
January 2, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29295991/network-connectivity-determines-cortical-thinning-in-early-parkinson-s-disease-progression
#3
Y Yau, Y Zeighami, T E Baker, K Larcher, U Vainik, M Dadar, V S Fonov, P Hagmann, A Griffa, B Mišić, D L Collins, A Dagher
Here we test the hypothesis that the neurodegenerative process in Parkinson's disease (PD) moves stereotypically along neural networks, possibly reflecting the spread of toxic alpha-synuclein molecules. PD patients (n = 105) and matched controls (n = 57) underwent T1-MRI at entry and 1 year later as part of the Parkinson's Progression Markers Initiative. Over this period, PD patients demonstrate significantly greater cortical thinning than controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex...
January 2, 2018: Nature Communications
https://www.readbyqxmd.com/read/29246765/fkbp12-immunopositive-inclusions-in-patients-with-%C3%AE-synucleinopathies
#4
Yasuyuki Honjo, Takashi Ayaki, Tomohisa Horibe, Hidefumi Ito, Ryosuke Takahashi, Koji Kawakami
α-Synuclein (α-SYN), a presynaptic protein with the tendency to aggregate, is linked to α-synucleinopathies such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA). α-SYN is the main component of round intracytoplasmic inclusions called Lewy bodies (LBs), which are the hallmark of PD and DLB. In addition, accumulation of amyloid-β and neurofibrillary tangles as in the pathology of Alzheimer's disease has been found in the DLB brain. Glial cytoplasmic inclusions are an MSA-specific type of inclusion found in oligodendrocytes and mainly comprise α-SYN...
December 12, 2017: Brain Research
https://www.readbyqxmd.com/read/29222591/dementia-with-lewy-bodies-and-parkinson-s-disease-dementia-current-concepts-and-controversies
#5
REVIEW
Kurt A Jellinger
Dementia with Lewy bodies (DLB) and Parkinson's disease-dementia (PDD), although sharing many clinical, neurochemical and morphological features, according to DSM-5, are two entities of major neurocognitive disorders with Lewy bodies of unknown etiology. Despite considerable clinical overlap, their diagnosis is based on an arbitrary distinction between the time of onset of motor and cognitive symptoms: dementia often preceding parkinsonism in DLB and onset of cognitive impairment after onset of motor symptoms in PDD...
December 8, 2017: Journal of Neural Transmission
https://www.readbyqxmd.com/read/29215728/multiple-neuronal-pathologies-are-common-in-young-patients-with-pathologically-proven-frontotemporal-lobar-degeneration
#6
Rachel H Tan, Yue Yang, Glenda M Halliday
AIMS: The past decade has seen a surge in studies identifying mixed pathologies in elderly populations. Importantly however, few studies have focussed on mixed pathology in Frontotemporal Lobar Degeneration (FTLD), particularly in younger cases. METHODS: The present study study examined concomitant pathological neuronal inclusions of TDP-43, hyperphosphorylated tau and α-synuclein protein in the anterior cingulate, hippocampus and entorhinal cortex in young (≤65 years at death) versus elderly (≥80 years at death) cases with pathologically-confirmed FTLD (n=52) or Alzheimer's disease (AD) (n=47)...
December 7, 2017: Neuropathology and Applied Neurobiology
https://www.readbyqxmd.com/read/29213490/neuropathological-findings-in-entorhinal-cortex-of-subjects-aged-50-years-or-older-and-their-correlation-with-dementia-in-a-sample-from-southern-brazil
#7
Edson Rodrigues Neto, Mariana K Fonseca, Álvaro C B Guedes, Francine H Oliveira, Arlete Hilbig, Liana Lisboa Fernandez
Introduction: The aims of this study were to survey neurodegenerative changes detected by abnormal protein deposits in the Entorhinal Cortex (EC) of subjects aged 50 years or older and to correlate these findings with suspected dementia, as detected by the IQCODE (Informant Questionnaire on Cognitive Decline in the Elderly). Methods: Fourteen brains were submitted to the immunohistochemistry technique for different proteins (beta-amyloid, tau, α-synuclein and phospho-TDP-43) and data obtained compared with IQCODE scores...
January 2017: Dementia & Neuropsychologia
https://www.readbyqxmd.com/read/29187283/new-insights-into-transglutaminase-2-and-links-to-neurodegenerative-diseases
#8
Boram Min, Kwang Chul Chung
Formation of toxic protein aggregates is a common feature and mainly contributes to the pathogenesis of neurodegenerative diseases (NDDs), which include amyotrophic lateral sclerosis (ALS), Alzheimer's, Parkinson's, Huntington's, and prion diseases. The transglutaminase 2 (TG2) gene encodes a multifunctional enzyme, displaying four types of activity, such as transamidation, GTPase, protein disulfide isomerase, and protein kinase activities. Many studies demonstrated that the calcium-dependent transamidation activity of TG2 affected the formation of insoluble and toxic amyloid aggregates that mainly consisted of NDD-related proteins...
November 29, 2017: BMB Reports
https://www.readbyqxmd.com/read/29186589/detergent-insoluble-proteins-and-inclusion-body-like-structures-immunoreactive-for-prkdc-dna-pk-dna-pkcs-ftl-nnt-and-aifm1-in-the-amygdala-of-cognitively-impaired-elderly-persons
#9
Jozsef Gal, Jing Chen, Yuriko Katsumata, David W Fardo, Wang-Xia Wang, Sergey Artiushin, Douglas Price, Sonya Anderson, Ela Patel, Haining Zhu, Peter T Nelson
Misfolded protein in the amygdala is a neuropathologic feature of Alzheimer disease and many other neurodegenerative disorders. We examined extracts from human amygdala (snap-frozen at autopsy) to investigate whether novel and as yet uncharacterized misfolded proteins would be detectable. Polypeptides from the detergent-insoluble, urea-soluble protein fractions of amygdala were interrogated using liquid chromatography-electrospray ionization-tandem mass spectrometry. Among the detergent-insoluble proteins identified in amygdala of demented subjects but not controls were Tau, TDP-43, Aβ, α-synuclein, and ApoE...
November 24, 2017: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/29186501/the-amygdala-as-a-locus-of-pathologic-misfolding-in-neurodegenerative-diseases
#10
Peter T Nelson, Erin L Abner, Ela Patel, Sonya Anderson, Donna M Wilcock, Richard J Kryscio, Linda J Van Eldik, Gregory A Jicha, Zsombor Gal, Ruth S Nelson, Bela G Nelson, Jozsef Gal, Md Tofial Azam, David W Fardo, Matthew D Cykowski
Over the course of most common neurodegenerative diseases the amygdala accumulates pathologically misfolded proteins. Misfolding of 1 protein in aged brains often is accompanied by the misfolding of other proteins, suggesting synergistic mechanisms. The multiplicity of pathogenic processes in human amygdalae has potentially important implications for the pathogenesis of Alzheimer disease, Lewy body diseases, chronic traumatic encephalopathy, primary age-related tauopathy, and hippocampal sclerosis, and for the biomarkers used to diagnose those diseases...
January 1, 2018: Journal of Neuropathology and Experimental Neurology
https://www.readbyqxmd.com/read/29177427/synaptic-phosphorylated-%C3%AE-synuclein-in-dementia-with-lewy-bodies
#11
Martí Colom-Cadena, Jordi Pegueroles, Abigail G Herrmann, Christopher M Henstridge, Laia Muñoz, Marta Querol-Vilaseca, Carla San Martín-Paniello, Joan Luque-Cabecerans, Jordi Clarimon, Olivia Belbin, Raúl Núñez-Llaves, Rafael Blesa, Colin Smith, Chris-Anne McKenzie, Matthew P Frosch, Allyson Roe, Juan Fortea, Jordi Andilla, Pablo Loza-Alvarez, Ellen Gelpi, Bradley T Hyman, Tara L Spires-Jones, Alberto Lleó
Dementia with Lewy bodies is characterized by the accumulation of Lewy bodies and Lewy neurites in the CNS, both of which are composed mainly of aggregated α-synuclein phosphorylated at Ser129. Although phosphorylated α-synuclein is believed to exert toxic effects at the synapse in dementia with Lewy bodies and other α-synucleinopathies, direct evidence for the precise synaptic localization has been difficult to achieve due to the lack of adequate optical microscopic resolution to study human synapses. In the present study we applied array tomography, a microscopy technique that combines ultrathin sectioning of tissue with immunofluorescence allowing precise identification of small structures, to quantitatively investigate the synaptic phosphorylated α-synuclein pathology in dementia with Lewy bodies...
December 1, 2017: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29172450/endogenous-alpha-synuclein-protein-analysis-from-human-brain-tissues-using-single-molecule-pull-down-assay
#12
Goun Je, Benjamin Croop, Sambuddha Basu, Jialei Tang, Kyu Young Han, Yoon-Seong Kim
Alpha-synuclein (α-SYN) is a central molecule in Parkinson's disease pathogenesis. Despite several studies, the molecular nature of endogenous α-SYN especially in human brain samples is still not well understood due to the lack of reliable methods and the limited amount of biospecimens. Here, we introduce α-SYN single-molecule pull-down (α-SYN SiMPull) assay combined with in vivo protein crosslinking to count individual α-SYN protein and assess its native oligomerization states from biological samples including human postmortem brains...
November 29, 2017: Analytical Chemistry
https://www.readbyqxmd.com/read/29159264/the-effects-of-apolipoprotein-e-genotype-%C3%AE-synuclein-deficiency-and-sex-on-brain-synaptic-and-alzheimer-s-disease-related-pathology
#13
Roni Bar, Anat Boehm-Cagan, Ishai Luz, Yarden Kleper-Wall, Daniel M Michaelson
Introduction: Alzheimer's disease (AD) and synucleinopathies share common pathological mechanisms. Apolipoprotein E4 (apoE4), the most prevalent genetic risk factor for AD, also increases the risk for dementia in pure synucleinopathies. We presently examined the effects of α-synuclein deficiency (α-syn-/-) and sex on apoE4-driven pathologies. Methods: AD-related, synaptic, and vascular markers were analyzed in female and male α-syn-/- and α-syn+/+ apoE4, apoE3, and apoE3/E4 mice...
2018: Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring
https://www.readbyqxmd.com/read/29151169/parkinson-s-disease-experimental-models-and-reality
#14
REVIEW
Peizhou Jiang, Dennis W Dickson
Parkinson's disease (PD) is a chronic, progressive movement disorder of adults and the second most common neurodegenerative disease after Alzheimer's disease. Neuropathologic diagnosis of PD requires moderate-to-marked neuronal loss in the ventrolateral substantia nigra pars compacta and α-synuclein (αS) Lewy body pathology. Nigrostriatal dopaminergic neurodegeneration correlates with the Parkinsonian motor features, but involvement of other peripheral and central nervous system regions leads to a wide range of non-motor features...
November 18, 2017: Acta Neuropathologica
https://www.readbyqxmd.com/read/29150334/a-routinely-used-protein-staining-dye-acts-as-an-inhibitor-of-wild-type-and-mutant-alpha-synuclein-aggregation-and-modulator-of-neurotoxicity
#15
Nuzhat Ahsan, Ibrar Ahmed Siddique, Sarika Gupta, Avadhesha Surolia
Inhibition of amyloid formation along with modulation of toxicity employing small molecules is emerging as a potential therapeutic approach for protein misfolding disorders which includes Parkinson's disease, Alzheimer's disease and Multiple System Atrophy etc. Countless current interventional strategies for treating α-synucleinopathies consider using peptidic and non-peptidic inhibitors for arresting fibrillisation, disrupting existing fibrils and reducing associated toxicity. One group of molecules less exploited in this regard are triphenylmethane dyes...
October 12, 2017: European Journal of Medicinal Chemistry
https://www.readbyqxmd.com/read/29147557/the-diversity-and-utility-of-amyloid-fibrils-formed-by-short-amyloidogenic-peptides
#16
REVIEW
Zahraa S Al-Garawi, Kyle L Morris, Karen E Marshall, Jutta Eichler, Louise C Serpell
Amyloidogenic peptides are well known for their involvement in diseases such as type 2 diabetes and Alzheimer's disease. However, more recently, amyloid fibrils have been shown to provide scaffolding and protection as functional materials in a range of organisms from bacteria to humans. These roles highlight the incredible tensile strength of the cross-β amyloid architecture. Many amino acid sequences are able to self-assemble to form amyloid with a cross-β core. Here we describe our recent advances in understanding how sequence contributes to amyloidogenicity and structure...
December 6, 2017: Interface Focus
https://www.readbyqxmd.com/read/29146111/microrna-expression-patterns-in-human-anterior-cingulate-and-motor-cortex-a-study-of-dementia-with-lewy-bodies-cases-and-controls
#17
Peter T Nelson, Wang-Xia Wang, Sarah A Janse, Katherine L Thompson
OVERVIEW: MicroRNAs (miRNAs) have been implicated in neurodegenerative diseases including Parkinson's disease and Alzheimer's disease (AD). Here, we evaluated the expression of miRNAs in anterior cingulate (AC; Brodmann area [BA] 24) and primary motor (MO; BA 4) cortical tissue from aged human brains in the University of Kentucky AD Center autopsy cohort, with a focus on dementia with Lewy bodies (DLB). METHODS: RNA was isolated from gray matter of brain samples with pathology-defined DLB, AD, AD+DLB, and low-pathology controls, with n=52 cases initially included (n=23 with DLB), all with low (<4hrs) postmortem intervals...
November 13, 2017: Brain Research
https://www.readbyqxmd.com/read/29130469/-heparan-sulphates-amyloidosis-and-neurodegeneration
#18
REVIEW
C Vera, J A Alvarez-Orozco, A Maiza, S Chantepie, R N Chehin, M O Ouidja, D Papy-Garcia
INTRODUCTION: A number of neurodegenerative disorders have been linked directly to the accumulation of amyloid fibres. These fibres are made up of proteins or peptides with altered structures and which join together in vivo in association with heparan sulphate-type polysaccharides. AIMS: To examine the most recent concepts in the biology of heparan sulphates and their role in the aggregation of the peptide Abeta, of tau protein, of alpha-synuclein and of prions...
November 16, 2017: Revista de Neurologia
https://www.readbyqxmd.com/read/29115515/serum-microrna-expression-profiling-in-patients-with-multiple-system-atrophy
#19
Kodai Kume, Hisakazu Iwama, Kazushi Deguchi, Kazuyo Ikeda, Tadayuki Takata, Yohei Kokudo, Masaki Kamada, Keiko Fujikawa, Kayo Hirose, Hisashi Masugata, Tetsuo Touge, Tsutomu Masaki
Multiple system atrophy (MSA) is a sporadic neurodegenerative disease that is pathologically characterized by α‑synuclein positive glial cytoplasmic inclusions in oligodendrocytes. The clinical diagnosis of MSA is often challenging as there are no established biomarkers and diagnoses are now based on clinical findings alone. At present, the etiology and pathogenesis of MSA are unclear. It has been reported that dysregulation of microRNA (miRNA/miR) serves an important role in neurodegenerative disorders including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis...
November 7, 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/29115353/lysophosphatidylcholine-modulates-the-aggregation-of-human-islet-amyloid-polypeptide
#20
Yanting Xing, Emily H Pilkington, Miaoyi Wang, Cameron J Nowell, Aleksandr Kakinen, Yunxiang Sun, Bo Wang, Thomas P Davis, Feng Ding, Pu Chun Ke
Amyloid aggregation of human islet amyloid polypeptide (IAPP) is a hallmark of type 2 diabetes (T2D), a metabolic disease and a global epidemic. Although IAPP is synthesized in pancreatic β-cells, its fibrils and plaques are found in the extracellular space indicating a causative transmembrane process. Numerous biophysical studies have revealed that cell membranes as well as model lipid vesicles promote the aggregation of amyloid-β (associated with Alzheimer's), α-synuclein (associated with Parkinson's) and IAPP, through electrostatic and hydrophobic interactions between the proteins/peptides and lipid membranes...
November 22, 2017: Physical Chemistry Chemical Physics: PCCP
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