Gangliosides, sialic acid-containing sphingolipids, are components of all mammalian cell membranes but are particularly abundant in neurons, where their concentration is up to ten times higher than that of non-neuronal cells. Hundreds of gangliosides have been identified with different expression patterns during development and are associated with various physiological processes, particularly in the nervous system.

There exists a significant connection between gangliosides and neurological disorders, as mutations that impair ganglioside biosynthesis enzymes can result in severe neurological disorders. Altered ganglioside levels are found in several neurodegenerative diseases (NDDs), such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis, and Huntington's disease. Currently, NDDs are the leading cause of dementia worldwide, affecting over fifty-five million people. During aging and neurodegeneration, the physicochemical properties of membranes are altered, resulting in imbalances in the composition of Gangliosides and altering neural function, subsequently leading to neuronal death. The human brain contains various types of gangliosides, with GM1a, GD1a, GD1b, and GT1b being the most prevalent.

Studies have revealed that individuals with Parkinson's disease have a 22% decrease in ganglioside content in their brains compared to healthy individuals, while those with Alzheimer's disease experience a 45% decline in ganglioside content. Exogenous application can restore ganglioside levels in lipid rafts and mimics the effects of growth factors in preventing cell death and survival of specific CNS cell populations, hence, ganglioside potential role as therapeutic agents has further enhanced.

Neuronal function and viability are critically dependent on Gangliosides, as evidenced by congenital mutations in ganglioside biosynthetic genes. For example, hereditary spastic paraplegia is caused by a disruption of B4GALNT1 gene. Another serious condition arising from disruption of ST3GAL5 gene, which codes for enzyme in ganglioside biosynthesis. Children with ST3GAL5 mutation have intellectual disability, choreoathetosis, visual and hearing impairments, failure to thrive, and dyspigmentation of the skin. Gangliosides also affect the aggregation of β Amyloid and α-synuclein proteins involved in Alzheimer's disease and Parkinson's Disease, respectively. Due to these implications, it is of utmost importance to understand how gangliosides can be used for neural repair and regeneration as well as therapeutic approaches, which focus on how genetic deletion or exogenous administration of one or more missing gangliosides can impart neuroprotection in various NDDs.

This research topic aims to focus on Neurodegenerative diseases and Gangliosides. The scope of this Research Topic includes but is not limited to:
-Therapeutic potential of exogenous ganglioside application
-Importance of gangliosides for neuronal viability and function
-The link between gangliosides and neurological disorders in NDDs
-Impact of aging and neurodegeneration on gangliosides and neural function
-Gangliosides in mammalian cell membranes and their role in neuronal physiology

We particularly welcome studies focusing on the role of ganglioside in cellular dysfunction and its potential therapeutic use. Authors are encouraged to submit Original Research, Reviews, and Perspective articles. Submissions solely investigating neuronal toxicity in cultured cells will not be taken into consideration.

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