The relationship between depletion of brain GM1 ganglioside and Parkinson's disease

Abstract

GM1 is one of the main gangliosides of the nervous system, and it exerts neurotrophic and neuroprotective properties in neurons. It is involved in many processes necessary for the correct physiology of neuronal cells. In particular, it is necessary for the activity of neuronal receptors that control processes such as differentiation, survival, and mitochondrial activity. A shortage of GM1 in the substantia nigra is potentially responsible for the neurodegeneration present in Parkinson's disease patients. In this review, I report on the role played by GM1 in neurons and how its genetic shortage may be responsible for the onset of Parkinson's disease.

An open chat with… Sandro Sonnino

“…The first Review article in this issue, authored by myself, describes the role of GM1 in neurons and how its depletion may contribute to the onset of Parkinson's disease [1]. This leads into the second Review article, authored by Fokion Spanos and Michela Deleidi, which discusses how changes in glycolipid metabolism can cause inflammatory reactions and contribute to Parkinson's disease and other neurodegenerative diseases [2]. Tatsuro Mutoh and colleagues then describe how disruptions in glycolipid and sphingolipid metabolism are observed in cases of encephalomyeloradiculoneuropathy (EMRN), which affects the brain, spinal cord, and peripheral nerves, and the involvement of such molecules in the immune system [3].…”

Alpha-Synuclein and GM1 Ganglioside Co-Localize in Neuronal Cytosol Leading to Inverse Interaction—Relevance to Parkinson’s Disease

“…Those studies demonstrated early involvement of the olfactory and autonomic components of the CNS and PNS, which often occur many years prior to observable movement disorders in both genetic and sporadic forms of PD. These and later manifestations of PD pathology derive from the progressive loss of dopaminergic (DA) neurons, along with other neuronal types, due at least in part to the accumulation of these misfolded, aggregated aSyn formations known to occur in PD patients as Lewy bodies and Lewy neurites [ 6 , 7 , 8 ]. Our work [ 9 , 10 ] and that of others [ 8 , 11 ] showed the systemic deficiency of GM1 ganglioside in the brain and periphery and proposed it as the underlying cause of such aSyn aggregation; this was based at least in part on the application of GM1 to various animal models of PD with striking therapeutic results [ 12 , 13 ].…”

Astaxanthin alleviates ganglioside metabolism disorder in the cortex of Alzheimer's disease mice

“…2 Abnormal changes in N-glycolylneuraminic acid (NeuGc) occurred in some human tissues that are inflammatory or cancerous. 5 As per the standard naming rules, G indicates a GLS structure, M/D/T/Q/P/H/S indicates the number of sialic acid units (1)(2)(3)(4)(5)(6)(7), and the difference obtained by subtracting the glycosyl number from the 5 represents the number of glycogroups in GLSs. The function of GLS may be related to the amount of sialic acid.…”

“…GM 1 , one of the main GLS of the nervous system, exhibits neurotrophic and neuroprotective properties in neurons. 6 The expression of GD 3 and GD 2 in † Electronic supplementary information (ESI) available. See DOI: https://doi.org/ 10.1039/d3fo03223j ‡ These authors contributed equally to this work.…”

“…GM 1 , one of the main GLS of the nervous system, exhibits neurotrophic and neuroprotective properties in neurons. 6 The expression of GD 3 and GD 2 in various cancers is predominantly upregulated and the increased expression is involved in tumor proliferation, invasion, metastasis, and immune responses. 7 GT 1b is vital for increasing the porcine oocyte nuclear maturation rate and decreasing intracellular ROS levels during in vitro maturation.…”