Galectins & Alpha-Synuclein

Galectins proteins bind to sugar molecules and mediate the cellular response to endocytic vesicles. It is believed that some galectin proteins are involved in microglia activation induced by α-synuclein. Here is the latest research on galectins and alpha-synuclein.

May 18, 2020
Open Access

Cardiovascular autonomic function testing in multiple system atrophy and Parkinson's disease: an expert-based blinded evaluation

Clinical Autonomic Research : Official Journal of the Clinical Autonomic Research Society
Fabian LeysGregor K Wenning
May 23, 2020

Astrocyte glutamate transporters are increased in an early sporadic model of synucleinopathy

Neurochemistry International
Luan Pereira DinizFlávia Carvalho Alcantara Gomes
May 31, 2020

Mesencephalic astrocyte-derived neurotrophic factor: A treatment option for parkinson's disease

Frontiers in Bioscience (Landmark Edition)
Chun Yang, Yan Gao
May 31, 2020
ReviewOpen Access

Degradation of Tyrosine Hydroxylase by the Ubiquitin-Proteasome System in the Pathogenesis of Parkinson's Disease and Dopa-Responsive Dystonia

International Journal of Molecular Sciences
Ichiro Kawahata, Kohji Fukunaga
May 19, 2020

Interlink between insulin resistance and neurodegeneration with an update on current therapeutic approaches

CNS & Neurological Disorders Drug Targets
Subrat Kumar BhattamisraHira Choudhury
May 24, 2020
Open Access

Increased alpha-synuclein tear fluid levels in patients with Parkinson's disease

Scientific Reports
Fabian MaassPaul Lingor
May 21, 2020

Association study of SNCA gene polymorphisms with schizophrenia in a Chinese North Han population

European Review for Medical and Pharmacological Sciences
X-P YangG Zhu
May 16, 2020
Open Access

Cerebrospinal Fluid Cytokines and Neurodegeneration-Associated Proteins in Parkinson's Disease

Movement Disorders : Official Journal of the Movement Disorder Society
Ruwani S WijeyekoonCaroline H Williams-Gray

Sign up to follow this feed and discover related papers.

Related Feeds

ALS

Amyotrophic Lateral Sclerosis (ALS), also known as motor neuron disease, is associated with the death of neurons that control voluntary muscles. Discover the latest research on ALS here.

ALS & FTD: TDP-43

ALS shares with a considerable proportion of FTD cases the same neuropathological substrate, namely, inclusions of abnormally phosphorylated protein tdp-43 (ptdp-43). Here are the latest discoveries pertaining to ptdp-43 and these diseases.

ALS - Pathogenic Mechanisms

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by muscle weakness. Here is the latest research investigating pathogenic mechanisms that underlie this genetically heterogeneous disorder.

ALS - Phenotypes

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by muscle weakness. Here is the latest research investigating phenotypes associated with this genetically heterogeneous disorder.

ALS: Genetics

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder characterized by muscle weakness. ALS is a genetically heterogeneous disorder with several causative genes. Here are the latest discoveries pertaining to the genetics of this disease.

ALS: Prions

Prions are misfolded proteins which characterize several fatal neurodegenerative diseases. Prion-like mechanisms are associated with the pathogenesis of Amyotrophic Lateral Sclerosis (ALS). Here are the latest discoveries pertaining to this disease.

ALS: Stress Granules

Amyotrophic Lateral Sclerosis (ALS) is a neurodegenerative disease characterized by cytoplasmic protein aggregates within motor neurons. TDP-43 is an ALS-linked protein that is known to regulate splicing and storage of specific mRNAs into stress granules, which have been implicated in formation of ALS protein aggregates. Here is the latest research.

ALS: Therapies

Amyotrophic Lateral Sclerosis (ALS), also known as motor neuron disease, is associated with the death of neurons that control voluntary muscles. Discover the latest research on ALS therapies here.

ALS: Transposon de-silencing

Transposon silencing is a form of transcriptional gene silencing. These gene silencing mechanisms are impaired in Amyotrophic lateral sclerosis (ALS). Here are the latest discoveries pertaining to transposon silencing and this disease.

Age-related Dementia

Age-related dementia (Alzheimer's disease) results from the destructive impact of the pulse on cerebral vasculature. Evidence is reviewed that the neuropathology of the dementia is caused by the breakdown of small cerebral vessels (silent microbleeds), that the microbleeds result from pulse-induced damage to the cerebral vessels, and that pulse becomes increasingly destructive with age, because of the age-related stiffening of the aorta and great arteries, which causes an increase in the intensity of the pressure pulse. Discover the latest research on age-related dementia here.

© 2020 Meta ULC. All rights reserved
/feed-previews/galectins-alpha-synuclein/a6062224-917a-497d-9fa9-90942e2f5c2f