☆ 4.6 Review

More than meets the eye in Parkinson's disease and other synucleinopathies: from proteinopathy to lipidopathy

ACTA NEUROPATHOLOGICA (2023)

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Review Clinical Neurology

Overexpression-Induced alpha-Synuclein Brain Spreading

Rita Pinto-Costa et al.

Summary: The transfer of pathological alpha-synuclein species between neurons is believed to be a key factor in the progression of Lewy pathology and the severity of clinical manifestations in synucleinopathies. However, the mechanisms underlying this trans-synaptic spreading are not fully understood. Animal models have shown that increased expression of alpha-synuclein can lead to its spreading throughout the brain and to peripheral tissues. Intriguing findings have also revealed the role of neuronal activity and oxidant stress in promoting interneuronal alpha-synuclein transfer.

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Article Biochemistry & Molecular Biology

The GBA variant E326K is associated with alpha-synuclein aggregation and lipid droplet accumulation in human cell lines

Laura J. Smith et al.

Summary: Sequence variants or mutations in the GBA gene are the most important risk factor for Parkinson's disease. This study characterizes the effects of the E326K variant in human cells and finds that it behaves differently compared to other common GBA mutations. However, lipid imbalance and alpha-synuclein pathology are still observed.

HUMAN MOLECULAR GENETICS (2023)

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Review Clinical Neurology

Overexpression-Induced α-Synuclein Brain Spreading

Rita Pinto-Costa et al.

Summary: The interneuronal transfer of pathological alpha-synuclein species is crucial in the progression of Lewy pathology and the severity of clinical manifestations in synucleinopathies. Animal models with alpha-synuclein overexpression have provided insights into the conditions and mechanisms that promote interneuronal alpha-synuclein transfer, including neuronal activity and oxidant stress.

NEUROTHERAPEUTICS (2023)

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Review Neurosciences

Potential treatment of Parkinson's disease with omega-3 polyunsaturated fatty acids

Peng Li et al.

Summary: Parkinson's disease is characterized by dysfunction of the nigrostriatal system, loss of dopamine neurons, and aggregation of alpha-synuclein. Neuroinflammation and oxidative stress play important roles in the development of Parkinson's disease. Polyunsaturated fatty acids, especially omega-3, have anti-inflammatory and neuroprotective effects, and may be a potential treatment for Parkinson's disease. This review discusses the effects of omega-3 PUFAs on Parkinson's disease in clinical patients and different models, and also explores the limitations and future research directions in this area.

NUTRITIONAL NEUROSCIENCE (2022)

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Review Biochemistry & Molecular Biology

Neuropathological Features of Gaucher Disease and Gaucher Disease with Parkinsonism

Makaila L. Furderer et al.

Summary: Deficiency of acid beta-glucocerebrosidase activity due to mutations in GBA1 causes Gaucher disease (GD). GD patients exhibit a wide range of symptoms, from asymptomatic adults to severe neurodegeneration. GBA1 variants are also important risk factors for several common Lewy body disorders (LBDs). Further neuropathological examinations in GD are needed to understand disease-specific patterns and mechanisms.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2022)

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Article Neurosciences

Glucocerebrosidase-associated Parkinson disease: Pathogenic mechanisms and potential drug treatments

Matthew E. Gegg et al.

Summary: Dysfunction of the endolysosomal system is associated with the pathogenesis of Parkinson's disease (PD), and genetic variants in the GBA gene are a common risk factor. GCase deficiency in neurons and glia may contribute to PD by promoting the accumulation and spread of alpha-synuclein aggregates. Dysregulation of lipids, including sphingolipids, phospholipids, and cholesterol, as well as neuroinflammation and the interaction between GCase and LRRK2 protein, are also implicated in PD pathogenesis.

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The neuroinflammatory role of glucocerebrosidase in Parkinson's disease

Ru-Xue Bo et al.

Summary: This review discusses the role of lysosomal enzyme glucocerebrosidase (GCase) in Parkinson's disease (PD) and the pathogenesis of PD. Deficient GCase can cause lysosomal dysfunction, leading to neuroinflammation and neuron damage, ultimately promoting the progression of PD.

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From kitchen to clinic: Pharmacotherapeutic potential of common spices in Indian cooking in age-related neurological disorders

Narges Norouzkhani et al.

Summary: This article summarizes the neuroprotective potential of common Indian spices widely used in Ayurveda, which may have positive effects in age-related neurological disorders.

FRONTIERS IN PHARMACOLOGY (2022)

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Review Biochemistry & Molecular Biology

Upstream lipid and metabolic systems are potential causes of Alzheimer's disease, Parkinson's disease and dementias

Oliver Cooper et al.

Summary: Brain health relies on adaptability and resetting after challenges. Neurodegeneration occurs when adaptability is restricted. Accumulation of lipids compromises adaptability in neural circuits. Treatment targeting lipid metabolism can restore adaptive homeostasis in individuals at risk of cognitive decline.

FEBS JOURNAL (2022)

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Article Multidisciplinary Sciences

Lysosomal exocytosis releases pathogenic α-synuclein species from neurons in synucleinopathy models

Ying Xue Xie et al.

Summary: This study demonstrates that pathogenic aggregates of alpha-Synuclein (alpha Syn) generated by neurons accumulate within neuronal lysosomes and are released via SNARE-dependent lysosomal exocytosis. These findings provide important insights into the release mechanism of aggregates and the spread of pathology in synucleinopathies.

NATURE COMMUNICATIONS (2022)

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Article Neurosciences

Lysosomal lipid alterations caused by glucocerebrosidase deficiency promote lysosomal dysfunction, chaperone-mediated-autophagy deficiency, and alpha-synuclein pathology

Alba Navarro-Romero et al.

Summary: This study generated human dopaminergic cell lines expressing common GBA mutations and GBA knockout to investigate their relationship with the abnormal accumulation of alpha-synuclein. The loss of GCase activity resulted in lysosomal dysfunction, impairing autophagy pathways and leading to the accumulation of alpha-synuclein.

NPJ PARKINSONS DISEASE (2022)

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Article Biochemistry & Molecular Biology

Observation of α-Synuclein Preformed Fibrils Interacting with SH-SY5Y Neuroblastoma Cell Membranes Using Scanning Ion Conductance Microscopy

Christina Feng et al.

Summary: By using scanning ion conductance microscopy (SICM), this study monitored the membrane changes induced by alpha-Syn preformed fibrils (PFFs) in neuroblastoma cells. The results showed that as the concentration of PFFs increased, the roughness of the cell membranes significantly increased, and noticeable protrusions with a more crystalline appearance were observed. Cell viability was slightly reduced, but not dependent on the dose.

ACS CHEMICAL NEUROSCIENCE (2022)

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Article Cell Biology

Genetic defects in the sphingolipid degradation pathway and their effects on microglia in neurodegenerative disease

Maria L. Allende et al.

Summary: Sphingolipids, crucial plasma membrane lipids and signaling molecules in the nervous system, are degraded in lysosomes. Mutations in degradative enzyme genes may lead to lysosomal accumulation of sphingolipids and severe neurodegenerative diseases. Microglia, involved in clearing sphingolipid-rich membranes, are affected by these mutations, underscoring defective sphingolipid clearance as a shared feature in neurodegenerative diseases.

CELLULAR SIGNALLING (2021)

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Article Biochemistry & Molecular Biology

GBA Mutations Influence the Release and Pathological Effects of Small Extracellular Vesicles from Fibroblasts of Patients with Parkinson's Disease

Silvia Cerri et al.

Summary: This study found that GCase deficiency promotes the release of EVs, leading to increased levels of phosphorylated alpha-syn inside fibroblasts from PD patients. This suggests that dysregulation of EV trafficking and mishandling of alpha-synuclein may play a role in GBA-associated PD.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2021)

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Article Clinical Neurology

Association study of MCCC1/LAMP3 and DGKQ variants with Parkinson's disease in patients of Malay ancestry

Jia Lun Lim et al.

Summary: The study found that variants in the MCCC1/LAMP3 loci, specifically rs10513789 and rs12637471, provide protection against PD in the Malay population, while the rs12493050 variant and the DGKQ gene rs11248060 variant showed no association with PD.

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Metabolomics of sebum reveals lipid dysregulation in Parkinson's disease

Eleanor Sinclair et al.

Summary: This study used metabolomics profiling to identify changes in lipids in the sebum of PD patients, with alterations related to the carnitine shuttle, sphingolipid metabolism, arachidonic acid metabolism, and fatty acid biosynthesis. The findings suggest sebum can be a potential source for identifying biomarkers for PD.

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The docking of synaptic vesicles on the presynaptic membrane induced by α-synuclein is modulated by lipid composition

Wing K. Man et al.

Summary: This study demonstrates how the docking of synaptic vesicles induced by alpha-Synuclein is modulated by changes in lipid composition typically observed in neurodegenerative diseases in an in vitro system.

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Lipidomics Prediction of Parkinson's Disease Severity: A Machine-Learning Analysis

Hila Avisar et al.

Summary: This study identified lipid signatures that can predict motor severity in PD, with certain lipid classes and species showing different relationships with severity in men and women. Predicting intermediate disease stages was more accurate, laying the groundwork for future research on the biological mechanisms linking specific lipids with PD severity.

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Recent Insights into the Interplay of Alpha-Synuclein and Sphingolipid Signaling in Parkinson's Disease

Joanna A. Motyl et al.

Summary: Molecular studies suggest that Parkinson's disease is a protein conformational disease involving the spread of alpha-synuclein pathology along the neuraxis. Pathogenic forms of alpha-synuclein induce oxidative stress, neuroinflammation, and protein alterations in neighboring cells, leading to increased toxicity and neurodegeneration. Maintaining homeostasis between bioactive sphingolipids is crucial in cell defense against oxidative stress, with a focus on sphingosine kinases and sphingosine-1-phosphate signaling as potential pharmacological targets for neurological diseases like PD.

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES (2021)

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Review Biochemistry & Molecular Biology

Ceramide Metabolism and Parkinson's Disease-Therapeutic Targets

Antia Custodia et al.

Summary: This article summarizes the role of ceramide in cellular processes and highlights its importance in neurodegenerative diseases, particularly in Parkinson's disease.

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Misfolded α-synuclein causes hyperactive respiration without functional deficit in live neuroblastoma cells

Cathryn L. Ugalde et al.

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Review Clinical Neurology

Exploring Sphingolipid Implications in Neurodegeneration

Alice V. Alessenko et al.

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Dopaminergic neurodegeneration induced by Parkinson's disease-linked G2019S LRRK2 is dependent on kinase and GTPase activity

An Phu Tran Nguyen et al.

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA (2020)

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Article Multidisciplinary Sciences

L444P Gba1 mutation increases formation and spread of α-synuclein deposits in mice injected with mouse α-synuclein pre-formed fibrils

Anna Migdalska-Richards et al.

PLOS ONE (2020)

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Role of VPS13, a protein with similarity to ATG2, in physiology and disease

Berrak Ugur et al.

CURRENT OPINION IN GENETICS & DEVELOPMENT (2020)

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Neurodegenerative diseases as proteinopathies-driven immune disorders

Fausta Ciccocioppo et al.

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Transcriptomic signatures of brain regional vulnerability to Parkinson's disease

Arlin Keo et al.

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Characterization of Brain Lysosomal Activities in GBA-Related and Sporadic Parkinson's Disease and Dementia with Lewy Bodies

Tim E. Moors et al.

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Cardiolipin Promotes Pore-Forming Activity of Alpha-Synuclein Oligomers in Mitochondrial Membranes

Stephanie Ghio et al.

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Lewy pathology in Parkinson's disease consists of crowded organelles and lipid membranes

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Sex-Related Abnormalities in Substantia Nigra Lipids in Parkinson's Disease

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Modulation of β-glucocerebrosidase increases α-synuclein secretion and exosome release in mouse models of Parkinson's disease

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α-Synuclein may cross-bridge v-SNARE and acidic phospholipids to facilitate SNARE-dependent vesicle docking

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Loss of VPS1 3C Function in Autosomal-Recessive Parkinsonism Causes Mitochondrial Dysfunction and Increases PINK1/Parkin-Dependent Mitophagy

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Metabolite and Peptide Levels in Plasma and CSF Differentiating Healthy Controls from Patients with Newly Diagnosed Parkinson's Disease

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