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dementia with lewy bodies and Parkinson's

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https://www.readbyqxmd.com/read/29332010/oligogenic-genetic-variation-of-neurodegenerative-disease-genes-in-980-postmortem-human-brains
#1
Michael J Keogh, Wei Wei, Juvid Aryaman, Ian Wilson, Kevin Talbot, Martin R Turner, Chris-Anne McKenzie, Claire Troakes, Johannes Attems, Colin Smith, Safa Al Sarraj, Chris M Morris, Olaf Ansorge, Stuart Pickering-Brown, Nick Jones, James W Ironside, Patrick F Chinnery
BACKGROUND: Several studies suggest that multiple rare genetic variants in genes causing monogenic forms of neurodegenerative disorders interact synergistically to increase disease risk or reduce the age of onset, but these studies have not been validated in large sporadic case series. METHODS: We analysed 980 neuropathologically characterised human brains with Alzheimer's disease (AD), Parkinson's disease-dementia with Lewy bodies (PD-DLB), frontotemporal dementia-amyotrophic lateral sclerosis (FTD-ALS) and age-matched controls...
January 13, 2018: Journal of Neurology, Neurosurgery, and Psychiatry
https://www.readbyqxmd.com/read/29330884/synapsin-iii-is-a-key-component-of-%C3%AE-synuclein-fibrils-in-lewy-bodies-of-pd-brains
#2
Francesca Longhena, Gaia Faustini, Tatiana Varanita, Michela Zaltieri, Vanessa Porrini, Isabella Tessari, Pietro Luigi Poliani, Cristina Missale, Barbara Borroni, Alessandro Padovani, Luigi Bubacco, Marina Pizzi, PierFranco Spano, Arianna Bellucci
Lewy bodies (LB) and Lewy neurites (LN), which are primarily composed of α-synuclein (α-syn), are neuropathological hallmarks of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). We recently found that the neuronal phosphoprotein synapsin III (syn III) controls dopamine release via cooperation with α-syn and modulates α-syn aggregation. Here, we observed that LB and LN, in the substantia nigra of PD patients and hippocampus of one subject with DLB, displayed a marked immunopositivity for syn III...
January 13, 2018: Brain Pathology
https://www.readbyqxmd.com/read/29324989/synaptic-markers-of-cognitive-decline-in-neurodegenerative-diseases-a-proteomic-approach
#3
Erika Bereczki, Rui M Branca, Paul T Francis, Joana B Pereira, Jean-Ha Baek, Tibor Hortobágyi, Bengt Winblad, Clive Ballard, Janne Lehtiö, Dag Aarsland
Cognitive changes occurring throughout the pathogenesis of neurodegenerative diseases are directly linked to synaptic loss. We used in-depth proteomics to compare 32 post-mortem human brains in the prefrontal cortex of prospectively followed patients with Alzheimer's disease, Parkinson's disease with dementia, dementia with Lewy bodies and older adults without dementia. In total, we identified 10 325 proteins, 851 of which were synaptic proteins. Levels of 25 synaptic proteins were significantly altered in the various dementia groups...
January 9, 2018: Brain: a Journal of Neurology
https://www.readbyqxmd.com/read/29311330/gba1-deficiency-negatively-affects-physiological-%C3%AE-synuclein-tetramers-and-related-multimers
#4
Sangjune Kim, Seung Pil Yun, Saebom Lee, George Essien Umanah, Veera Venkata Ratnam Bandaru, Xiling Yin, Peter Rhee, Senthilkumar S Karuppagounder, Seung-Hwan Kwon, Hojae Lee, Xiaobo Mao, Donghoon Kim, Akhilesh Pandey, Gabsang Lee, Valina L Dawson, Ted M Dawson, Han Seok Ko
Accumulating evidence suggests that α-synuclein (α-syn) occurs physiologically as a helically folded tetramer that resists aggregation. However, the mechanisms underlying the regulation of formation of α-syn tetramers are still mostly unknown. Cellular membrane lipids are thought to play an important role in the regulation of α-syn tetramer formation. Since glucocerebrosidase 1 (GBA1) deficiency contributes to the aggregation of α-syn and leads to changes in neuronal glycosphingolipids (GSLs) including gangliosides, we hypothesized that GBA1 deficiency may affect the formation of α-syn tetramers...
January 8, 2018: Proceedings of the National Academy of Sciences of the United States of America
https://www.readbyqxmd.com/read/29310663/%C3%AE-synuclein-accumulation-and-gba-deficiency-due-to-l444p-gba-mutation-contributes-to-mptp-induced-parkinsonism
#5
Seung Pil Yun, Donghoon Kim, Sangjune Kim, SangMin Kim, Senthilkumar S Karuppagounder, Seung-Hwan Kwon, Saebom Lee, Tae-In Kam, Suhyun Lee, Sangwoo Ham, Jae Hong Park, Valina L Dawson, Ted M Dawson, Yunjong Lee, Han Seok Ko
BACKGROUND: Mutations in glucocerebrosidase (GBA) cause Gaucher disease (GD) and increase the risk of developing Parkinson's disease (PD) and Dementia with Lewy Bodies (DLB). Since both genetic and environmental factors contribute to the pathogenesis of sporadic PD, we investigated the susceptibility of nigrostriatal dopamine (DA) neurons in L444P GBA heterozygous knock-in (GBA +/L444P ) mice to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a selective dopaminergic mitochondrial neurotoxin...
January 8, 2018: Molecular Neurodegeneration
https://www.readbyqxmd.com/read/29305919/pathological-role-of-lipid-interaction-with-%C3%AE-synuclein-in-parkinson-s-disease
#6
REVIEW
Mari Suzuki, Kazunori Sango, Keiji Wada, Yoshitaka Nagai
Alpha-synuclein (αSyn) plays a central role in the pathogenesis of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). In sporadic PD and DLB, normally harmless αSyn proteins without any mutations might gain toxic functions by unknown mechanisms. Thus, it is important to elucidate the factors promoting the toxic conversion of αSyn, towards understanding the pathogenesis of and developing disease-modifying therapies for PD and DLB. Accumulating biophysical and biochemical studies have demonstrated that αSyn interacts with lipid membrane, and the interaction influences αSyn oligomerization and aggregation...
January 3, 2018: Neurochemistry International
https://www.readbyqxmd.com/read/29305061/a-refined-concept-alpha-synuclein-dysregulation-disease
#7
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/29297596/neuropathology-of-autonomic-dysfunction-in-synucleinopathies
#8
REVIEW
Elizabeth A Coon, Jeremy K Cutsforth-Gregory, Eduardo E Benarroch
The synucleinopathies-Parkinson's disease, dementia with Lewy bodies, multiple system atrophy, and pure autonomic failure-result from distinct patterns of abnormal α-synuclein aggregation throughout the nervous system. Autonomic dysfunction in these disorders results from variable involvement of the central and peripheral autonomic networks. The major pathologic hallmark of Parkinson's disease and dementia with Lewy bodies is Lewy bodies and Lewy neurites; of multiple system atrophy, oligodendroglial cytoplasmic inclusions; and of pure autonomic failure, peripheral neuronal cytoplasmic inclusions...
January 3, 2018: Movement Disorders: Official Journal of the Movement Disorder Society
https://www.readbyqxmd.com/read/29261640/the-added-value-of-dynamic-18f-florbetapir-pet-in-the-assessment-of-dementia-with-lewy-bodies
#9
Diego Alfonso López Mora, Valle Camacho, Alberto Lleó, Alejandro Fernández, Ignasi Carrió
Dementia with Lewy bodies (DLB) is the most common cause of dementia after Alzheimer disease. It is often underdiagnosed because of the overlapping with Alzheimer disease symptoms. We report the F-FDG and F-florbetapir dynamic PET images (early and delay phases) of an 83-year-old woman with cognitive impairment associated with visual hallucinations and parkinsonism due to probable DLB. This image highlights that the early phases of F-florbetapir may reflect regional cerebral perfusion with a pattern very similar to that of regional glucose metabolism in DLB...
December 19, 2017: Clinical Nuclear Medicine
https://www.readbyqxmd.com/read/29246926/combined-active-humoral-and-cellular-immunization-approaches-for-the-treatment-of-synucleinopathies
#10
Edward Rockenstein, Gary Ostroff, Fusun Dikengil, Florentina Rus, Michael Mante, Jazmin Florio, Anthony Adame, Ivy Trinh, Changyoun Kim, Cassia Overk, Eliezer Masliah, Robert A Rissman
Dementia with Lewy bodies (DLB), Parkinson's disease (PD) and Multiple System Atrophy (MSA) are age-related neurodegenerative disorders characterized by progressive accumulation of α-synuclein (α-syn) and jointly termed synucleinopathies. Currently, no disease-modifying treatments are available for these disorders. Previous preclinical studies showed that active and passive immunizations targeting α-syn partially ameliorates behavioral deficits and α-syn accumulation; however, it is unknown if combining humoral and cellular immunization might act synergistically to reduce inflammation and improve microglial-mediated α-syn clearance...
December 15, 2017: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
https://www.readbyqxmd.com/read/29246765/fkbp12-immunopositive-inclusions-in-patients-with-%C3%AE-synucleinopathies
#11
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/29240340/update-on-current-care-guideline-memory-disorders
#12
(no author information available yet)
Any complaint about memory should be examined. Diagnosis is based on international criteria. Basic evaluation consists of medical history, clinical evaluation, cognitive tests and brain imaging. When a diagnosis of Alzheimer's disease (AD), AD with cerebrovascular disease or with Lewy Body disease (LBD), or Dementia associated with Parkinson's disease or LBD is made, evidence-based medical therapy (acetylcholine esterase inhibitor or memantine) is indicated as a part of comprehensive care. In frontotemporal degenerations, these drugs are ineffective...
2017: Duodecim; Lääketieteellinen Aikakauskirja
https://www.readbyqxmd.com/read/29228071/associations-between-tau-%C3%AE-amyloid-and-cognition-in-parkinson-disease
#13
Joseph R Winer, Anne Maass, Peter Pressman, Jordan Stiver, Daniel R Schonhaut, Suzanne L Baker, Joel Kramer, Gil D Rabinovici, William J Jagust
Importance: Multiple disease processes are associated with cognitive impairment in Parkinson disease (PD), including Lewy bodies, cerebrovascular disease, and Alzheimer disease. It remains unknown whether tau pathology relates to cognition in patients with PD without dementia. Objective: To compare tau aggregation in patients with PD who are cognitively normal (PD-CN), patients with PD with mild cognitive impairment (PD-MCI), and healthy control participants, and evaluate the relationships between β-amyloid (Aβ), tau, and cognition in patients with PD who did not have dementia...
December 11, 2017: JAMA Neurology
https://www.readbyqxmd.com/read/29222591/dementia-with-lewy-bodies-and-parkinson-s-disease-dementia-current-concepts-and-controversies
#14
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/29216908/clinical-and-neuropathological-features-of-als-ftd-with-tia1-mutations
#15
Veronica Hirsch-Reinshagen, Cyril Pottier, Alexandra M Nicholson, Matt Baker, Ging-Yuek R Hsiung, Charles Krieger, Pheth Sengdy, Kevin B Boylan, Dennis W Dickson, Marsel Mesulam, Sandra Weintraub, Eileen Bigio, Lorne Zinman, Julia Keith, Ekaterina Rogaeva, Sasha A Zivkovic, David Lacomis, J Paul Taylor, Rosa Rademakers, Ian R A Mackenzie
Mutations in the stress granule protein T-cell restricted intracellular antigen 1 (TIA1) were recently shown to cause amyotrophic lateral sclerosis (ALS) with or without frontotemporal dementia (FTD). Here, we provide detailed clinical and neuropathological descriptions of nine cases with TIA1 mutations, together with comparisons to sporadic ALS (sALS) and ALS due to repeat expansions in C9orf72 (C9orf72+). All nine patients with confirmed mutations in TIA1 were female. The clinical phenotype was heterogeneous with a range in the age at onset from late twenties to the eighth decade (mean = 60 years) and disease duration from one to 6 years (mean = 3 years)...
December 7, 2017: Acta Neuropathologica Communications
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
#16
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...
December 4, 2017: Autophagy
https://www.readbyqxmd.com/read/29196808/propagation-of-alpha-synuclein-pathology-from-the-olfactory-bulb-possible-role-in-the-pathogenesis-of-dementia-with-lewy-bodies
#17
REVIEW
María Graciela Cersosimo
Olfactory limbic structures, like the amygdala, the entorhinal, and the piriform cortices, are closely involved in cognitive processes. Thus, besides olfactory dysfunctions, it is conceivable that the compromise of these structures can lead to cognitive impairment. The olfactory bulb is affected by alpha-synuclein pathology in almost all cases of both Parkinson's disease and dementia with Lewy bodies. The clinical distinction between these disorders relies on the timing in the appearance of dementia in relationship to motor symptoms...
December 1, 2017: Cell and Tissue Research
https://www.readbyqxmd.com/read/29195744/discrimination-of-atypical-parkinsonisms-with-transcranial-magnetic-stimulation
#18
Alberto Benussi, Valentina Dell'Era, Valentina Cantoni, Clarissa Ferrari, Salvatore Caratozzolo, Luca Rozzini, Antonella Alberici, Alessandro Padovani, Barbara Borroni
BACKGROUND: Differential diagnosis of atypical parkinsonian disorders, i.e. dementia with Lewy bodies (DLB), progressive supranuclear palsy (PSP) or corticobasal syndrome (CBS) still remains problematic. Furthermore, DLB may overlap with Alzheimer's disease (AD) in the early stages of disease. OBJECTIVE: To determine whether transcranial magnetic stimulation (TMS) can be used to classify atypical parkinsonian disorders and AD. METHODS: A paired-pulse TMS multi-paradigm approach assessing multiple intracortical circuits, as short interval intracortical inhibition-facilitation and short latency afferent inhibition, was used to model a decision tree analysis and determine diagnostic accuracy in classifying different neurodegenerative disorders...
November 22, 2017: Brain Stimulation
https://www.readbyqxmd.com/read/29193464/functional-connectivity-in-dementia-with-lewy-bodies-a-within-and-between-network-analysis
#19
Julia Schumacher, Luis R Peraza, Michael Firbank, Alan J Thomas, Marcus Kaiser, Peter Gallagher, John T O'Brien, Andrew M Blamire, John-Paul Taylor
Dementia with Lewy bodies (DLB) is a common form of dementia and is characterized by cognitive fluctuations, visual hallucinations, and Parkinsonism. The phenotypic expression of the disease may, in part, relate to alterations in functional connectivity within and between brain networks. This resting-state study sought to clarify this in DLB, how networks differed from Alzheimer's disease (AD), and whether they were related to clinical symptoms in DLB. Resting-state networks were estimated using independent component analysis...
November 29, 2017: Human Brain Mapping
https://www.readbyqxmd.com/read/29187334/cognitive-profile-in-prodromal-disease-dementia-with-lewy-bodies
#20
Jennifer Kemp, Nathalie Philippi, Clélie Phillipps, Anne Botzung, Frédéric Blanc
This paper reviews findings on cognition in prodromal dementia with Lewy bodies (DLB). The issue of differential diagnosis between DLB and Alzheimer's disease (AD) on the one hand, and Parkinson's disease (PD) on the other hand, at prodromal stages of the diseases is discussed. The cognitive profile of prodromal DLB is also evaluated in terms of cognitive deficits and « cognitive weaknesses » (low performances although in normal range). Findings suggest that visuo-constructive tests and verbal fluency are particularly relevant to dfferentiate DLB from AD...
December 1, 2017: Gériatrie et Psychologie Neuropsychiatrie du Vieillissement
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