Synuclein

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Synuclein

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46 items · Synuclein

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SeminarNeuroscience

The synaptic functions of Alpha Synuclein and Lrrk2

Subhojit Roy, MD, PhD

University of Wisconsin-Madison

Feb 17, 2025

Alpha synuclein and Lrrk2 are key players in Parkinson's disease and related disorders, but their normal role has been confusing and controversial. Data from acute gene-editing based knockdown, followed by functional assays, will be presented.

SeminarNeuroscience

Alpha synuclein in parkinson's Disease: From the bedside to the bench and back again

Stefanis Leonidas

Medical School, National and Kapodistrian University of Athens and Biomedical Research Foundation of the Academy of Athens, Athens, Greece

Jan 30, 2024

SeminarNeuroscience

Multimodal imaging in Dementia with Lewy bodies

Kejal Kantarci

Mayo Clinic

Feb 13, 2022

Dementia with Lewy bodies (DLB) is a synucleinopathy but more than half of patients with DLB also have varying degrees of tau and amyloid-β co-pathology. Identifying and tracking the pathologic heterogeneity of DLB with multi-modal biomarkers is critical for the design of clinical trials that target each pathology early in the disease at a time when prevention or delaying the transition to dementia is possible. Furthermore, longitudinal evaluation of multi-modal biomarkers contributes to our understanding of the type and extent of the pathologic progression and serves to characterize the temporal emergence of the associated phenotypic expression. This talk will focus on the utility of multi-modal imaging in DLB.

SeminarNeuroscience

Multimorbidity in the ageing human brain: lessons from neuropathological assessment

Kirsty McAleese

Newcastle University

Jun 7, 2021

Age-associated dementias are neuropathologically characterized by the identification of hallmark intracellular and extracellular deposition of proteins, i.e., hyperphosphorylated-tau, amyloid-β, and α-synuclein, or cerebrovascular lesions. The neuropathological assessment and staging of these pathologies allows for a diagnosis of a distinct disease, e.g., amyloid-β plaques and hyperphosphorylated tau pathology in Alzheimer's disease. Neuropathological assessment in large scale cohorts, such as the UK’s Brains for Dementia Research (BDR) programme, has made it increasingly clear that the ageing brain is characterized by the presence of multiple age-associated pathologies rather than just the ‘pure’ hallmark lesion as commonly perceived. These additional pathologies can range from low/intermediate levels, that are assumed to have little if any clinical significance, to a full-blown mixed disease where there is the presence of two distinct diseases. In our recent paper (McAleese et al. 2021 Concomitant neurodegenerative pathologies contribute to the transition from mild cognitive impairment to dementia, https://alz-journals.onlinelibrary.wiley.com/doi/full/10.1002/alz.12291, Alzheimer's & Dementia), using the BDR cohort, we investigated the frequency of multimorbidity and specifically investigated the impact of additional low-level pathology on cognition. In this study, of 670 donated post-mortem brains, we found that almost 70% of cases exhibited multimorbidity and only 22% were considered a pure diagnosis. Importantly, no case of Lewy Body dementia or vascular dementia was considered pure. A key finding is that the presence of low levels of additional pathology increased the likelihood of having mild dementia vs mild cognitive impairment by almost 20-fold, indicating low levels of additional pathology do impact the clinical progression of a distinct disease. Given the high prevalence and the potential clinical impact, cerebral multimorbidity should be at the forefront of consideration in dementia research.

SeminarNeuroscience

Targeting selective autophagy against neurodegenerative diseases

Ana Maria Cuervo

Albert Einstein College of Medicine, New York, USA

Apr 20, 2021

Protein quality control is essential for maintenance of a healthy and functional proteome that can attend the multiplicity of cellular functions. Failure of the systems that contribute to protein homeostasis, the so called proteostasis networks, have been identified in the pathogenesis of multiple neurodegenerative disorders and demonstrated to contribute to disease onset and progression. We are interested in autophagy, one of the components of the proteostasis network, and in the interplay of wo selective types of autophagy, chaperone-mediated autophagy (CMA) and endosomal microautophagy (eMI), with neurodegeneration. We have recently found that pathogenic proteins involved in common neurodegenerative conditions such as tauopathies or Parkinson’s disease, can exert a toxic effect in both types of selective types of autophagy compromising their functioning. We have now used mouse models with compromised CMA that support increased propagation of proteins such as tau and alpha-synuclein and an exacerbation of disease phenotype with aging. Conversely, genetic or chemical upregulation of CMA in this context of proteotoxicity slow down disease progression by facilitating effective intracellular removal of pathogenic proteins. Our findings highlight CMA and eMI as potential novel therapeutic targets against neurodegeneration.

SeminarNeuroscience

Neurotoxicity is a major health problem in Africa: focus on Parkinson's / Parkinsonism

Nouria Lakhdar-Ghazal

Mohammed V University, Morocco

Oct 21, 2020

Parkinson's disease (PD) is the second most present neurodegenerative disease in the world after Alzheimer's. It is due to the progressive and irreversible loss of dopaminergic neurons of the substantia nigra Pars Compacta. Alpha synuclein deposits and the appearance of Lewi bodies are systematically associated with it. PD is characterized by four cardinal motor symptoms: bradykinesia / akinesia, rigidity, postural instability and tremors at rest. These symptoms appear when 80% of the dopaminergic endings disappear in the striatum. According to Braak's theory, non-motor symptoms appear much earlier and this is particularly the case with anxiety, depression, anhedonia, and sleep disturbances. In 90 to 95% of cases, the causes of the appearance of the disease remain unknown, but polluting toxic molecules are incriminated more and more. In Africa, neurodegenerative diseases of the Parkinson's type are increasingly present and a parallel seems to exist between the increase in cases and the presence of toxic and polluting products such as metals. My Web conference will focus on this aspect, i.e. present experimental arguments which reinforce the hypothesis of the incrimination of these pollutants in the incidence of Parkinson's disease and / or Parkinsonism. Among the lines of research that we have developed in my laboratory in Rabat, Morocco, I have chosen this one knowing that many of our PhD students and IBRO Alumni are working or trying to develop scientific research on neurotoxicity in correlation with pathologies of the brain.

Synuclein

Synuclein

The synaptic functions of Alpha Synuclein and Lrrk2

Alpha synuclein in parkinson's Disease: From the bedside to the bench and back again

Multimodal imaging in Dementia with Lewy bodies

Multimorbidity in the ageing human brain: lessons from neuropathological assessment

Targeting selective autophagy against neurodegenerative diseases

Neurotoxicity is a major health problem in Africa: focus on Parkinson's / Parkinsonism

α-Synuclein propagation leads to synaptic abnormalities in the cortex through microglial synapse phagocytosis

AAV-mediated overexpression of wild-type human alpha-synuclein leads to alterations in gut microbiota in a ‘brain-first’ rat model of prodromal Parkinson’s disease

Accumulation of phospho-alpha synuclein and oligomeric tau in presynapses in Parkinson’s disease and Dementia with Lewy Bodies

Alpha-synuclein induced immune response triggers Parkinson’s disease

Alpha-synuclein pathology from human-derived Lewy body inoculations in the mouse olfactory bulb: Modelling early Parkinson’s disease

Altered firing and dopamine release in Substantia Nigra dopaminergic neurons induced by exposure to alpha-synuclein oligomers: From patch-clamp to diamond multielectrode arrays

Amyloid beta 1-42 and alpha-synuclein proteins: Effects on transcription factor expression

Cellular and molecular characterization of serotonergic synapses in a mouse model of depression and raphe synucleinopathy

Corticostriatal overactivity and alpha-synuclein overexpression produce striatal astrocytosis in mice

DAD9, a novel agonist concept that breaks the lethal partnership between α-synuclein and dopamine

Depressive and anxious phenotype correlates with functional changes in the ventromedial prefrontal cortex - dorsal raphe nucleus circuit in female mice with alpha-synucleinopathy

Depressive-like phenotype induced by AAV-mediated overexpression of human α-synuclein in midbrain dopaminergic neurons

Differences in the synaptic function of human and murine alpha-synuclein

Dose-dependent effect of alpha-synuclein overexpression on neuronal cells

Effect of alpha-synuclein on the expression of genes encoded in mitochondrial DNA

Effects of AAV-GDNF and AAV-GDF5 in an AAV-α-synuclein rat model of Parkinson’s disease

Effects of alpha-synuclein on dopamine and serotonin transporters

Exercise-based rescue strategies for early striatal synaptic impairment and motor abnormalities caused by alpha-synuclein

Endogenous alpha-Synuclein is essential for the transfer of pathology by exosome-enriched extracellular vesicles, following inoculation with preformed fibrils in vivo

Evidence of prodromal neuronal hyperexcitability and neuroinflammation in a rodent model of human alpha-synucleinopathy

Exploring the interplay of gait and anxiety in a synucleinopathy model of Parkinson’s disease

Extracellular vesicles and transmission of α-synuclein pathology: From cellular models to diagnostic applications

FoxO1 induced by alpha-synuclein preformed fibrils regulates ROS by expressing antioxidant genes in microglia

Functional, behavioural and molecular characterization of a presymptomatic model of Parkinson disease expressing α-synuclein in the locus coeruleus

Glucocerebrosidase pharmacological chaperones attenuate α-synuclein-induced neurotoxicity in chronic cortico-striatal slices

Glucocorticoid receptors in astrocytes regulate alpha-synuclein pathological actions impacting motor and non-motor symptomatology of Parkinson's disease

Increased fear-related behaviors following alpha-synuclein preformed fibrils injected into the basolateral amygdala or striatum in mice

Inhibition of nuclear-retained HDAC5 interactome prevents neurite degeneration induced by α-synuclein overexpression

Investigating changes in interneurons and perineuronal nets in a rodent model of alpha-synucleinopathy

Investigating gut-microbe interactions and epithelial α-synuclein through human enteroid monolayers and imaging flow cytometry of enteroendocrine cells in vitro

miR-302 induced by glucagon-like peptide-1 (GLP-1) signaling reduces the α-synuclein neurotoxicity linked to dementia with Lewy bodies (DLB)

Neurotoxic effect of viral RNA-mimetic and alpha-synuclein in neuronal-glia co-cultures

Novel viral vectors for cell-type specific overexpression of alpha-synuclein

Oligomeric alpha-synuclein causes early striatal synaptic dysfunction associated with non-motor symptoms

Overexpression-induced nuclear alpha-synuclein accumulation

Partners in crime: Alpha-synuclein and Tau co-aggregation impairs microglial function during Parkinson’s disease

Pharmacological modulation of Nrf2 pathway in alpha-synuclein mouse model of Parkinson’s disease

Repurposing pomalidomide as a neuroprotective drug in an alpha-synuclein-based model of Parkinson’s disease

Resolving molecular structures in α-synuclein and Tau cross-seeding with novel super-resolution infrared imaging

The role of EEF1A proteins at synapses and in synucleinopathy