Results 161 to 170 of about 91,122 (346)

GM1 Ganglioside Modifies α-Synuclein Toxicity and is Neuroprotective in a Rat α-Synuclein Model of Parkinson\u27s Disease. [PDF]

open access: yes, 2019
While GM1 may interact with α-synuclein in vitro to inhibit aggregation, the ability of GM1 to protect against α-synuclein toxicity in vivo has not been investigated.
Aras, Radha   +5 more
core   +1 more source

Pathogenic or Likely Pathogenic GRN Variants Are Found in 0.1% of Parkinson's Disease Patients

open access: yesMovement Disorders, EarlyView.
Abstract Background Parkinsonism may be observed in multiple neurodegenerative diseases, including GRN‐associated frontotemporal dementia (FTD‐GRN), complicating the differential diagnosis of Parkinson's disease (PD). Objectives To investigate the presence of GRN variants in a large group of PD patients.
Christian A. Ganoza   +31 more
wiley   +1 more source

Diagnostic Value of Bedside Eye Movement Examination in Movement Disorders

open access: yes
Movement Disorders Clinical Practice, EarlyView.
Eloísa Bittencurt Thomaz de Assis   +4 more
wiley   +1 more source

Uncovering the Complexity of Synucleinopathies: An Ongoing Tale Between Proteins and Lipids

open access: yesMovement Disorders, EarlyView.
Abstract Neurodegenerative diseases are pathological states characterized by progressive alterations in brain homeostasis during aging. Synucleinopathies, including Parkinson's disease and dementia with Lewy bodies, are defined neuropathologically by the accumulation of inclusions known as Lewy bodies and Lewy neurites.
Manuel Flores‐León, Tiago F. Outeiro
wiley   +1 more source

The Race to Salvage Glucocerebrosidase: Understanding Small‐Molecule Therapies for GBA1‐Associated Parkinsonism

open access: yesMovement Disorders, EarlyView.
Variants in GBA1, the gene encoding the lysosomal enzyme glucocerebrosidase, cause Gaucher disease and confer an increased risk for parkinsonism. Strategies using small molecules can improve the function of glucocerebrosidase in lysosomes. A clear understanding of the mechanism‐of‐action of these compounds will facilitate development of GBA1‐modulating
Mark J. Henderson   +5 more
wiley   +1 more source

Discordance of Dopaminergic Dysfunction and Subcortical Atrophy by α‐Synuclein Status in Sporadic and Genetic Parkinson's Disease

open access: yesMovement Disorders, EarlyView.
Abstract Background Parkinson's disease (PD) is characterized by predominantly neuronal α‐synuclein pathology and dopaminergic dysfunction. Cerebrospinal fluid (CSF) seeding amplification assays (SAA) detect α‐synuclein aggregates in vivo, but not all patients with PD have a positive SAA.
Michael Tran Duong   +186 more
wiley   +1 more source

Fluctuating cognition in the Lewy body dementias [PDF]

open access: bronze, 2019
Seán O’Dowd   +6 more
openalex   +1 more source

Perampanel Blocks Transsynaptic α‐Synuclein Propagation and Neurodegeneration in a Mouse Model of Lewy Body Disease

open access: yesMovement Disorders, EarlyView.
Abstract Background Transsynaptic α‐synuclein propagation plays a crucial role in the progression of Lewy body disease. We previously demonstrated that an α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid receptor antagonist, perampanel, blocks neuronal uptake of α‐synuclein preformed fibrils (PFFs) in an activity‐dependent manner.
Jun Ueda   +9 more
wiley   +1 more source

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