Sweet Aging : Glycocalyx and Galectins in CNS Aging and Neurodegenerative Disorders
Mir, Mohd Yaqub LU
and Legradi, Adam
(2025)
In International Journal of Molecular Sciences
26(10).
- Abstract
Aging and aging-related neurodegenerative disorders, such as Alzheimer’s disease, are characterized by chronic inflammation that progressively damages nervous tissue within the central nervous system (CNS). In addition to cytokines, lectin-like carbohydrate recognition molecules play a critical role in modifying cellular communication during inflammation. Among these, galectins—particularly anti-inflammatory galectin-1 and pro-inflammatory galectin-3—stand out due to their immunological functions and specificity for N-acetyllactosamine structures. Almost every cell type within the CNS can express and recognize galectins, influencing various essential cellular functions. N-acetyllactosamines, the ligand structures recognized by... (More)
Aging and aging-related neurodegenerative disorders, such as Alzheimer’s disease, are characterized by chronic inflammation that progressively damages nervous tissue within the central nervous system (CNS). In addition to cytokines, lectin-like carbohydrate recognition molecules play a critical role in modifying cellular communication during inflammation. Among these, galectins—particularly anti-inflammatory galectin-1 and pro-inflammatory galectin-3—stand out due to their immunological functions and specificity for N-acetyllactosamine structures. Almost every cell type within the CNS can express and recognize galectins, influencing various essential cellular functions. N-acetyllactosamines, the ligand structures recognized by galectins, are found beneath sialylated termini in protein-linked oligosaccharides. During aging, protein-linked oligosaccharide structures become shorter, exposing N-acetyllactosamines on protein surfaces, which enhances their availability as binding sites for galectins. Genomic studies indicate that the number of galectin-1- and galectin-3-expressing microglial cells increases with age- or age-related disease (Alzheimer’s disease), reflecting an aging-associated rise in galectin concentrations within the CNS. This increase parallels a rise in free N-acetyllactosamine-like ligands, suggesting that galectin-N-acetyllactosamine interactions gain prominence and play a more significant role in aging-related CNS disorders. Understanding these interactions and their molecular implications offers potential avenues for targeted therapeutic strategies in combating aging-related CNS inflammation and neurodegeneration.
(Less)
- author
- Mir, Mohd Yaqub
LU
and Legradi, Adam
- organization
- publishing date
- 2025-05
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- aging, galectins, glycan–lectin interaction, neuroinflammation
- in
- International Journal of Molecular Sciences
- volume
- 26
- issue
- 10
- article number
- 4699
- publisher
- MDPI AG
- external identifiers
-
- pmid:40429840
- scopus:105006693439
- ISSN
- 1661-6596
- DOI
- 10.3390/ijms26104699
- language
- English
- LU publication?
- yes
- id
- 5dd7470b-b975-4a53-bb1b-283025ba3012
- date added to LUP
- 2025-08-04 10:32:59
- date last changed
- 2025-08-05 03:34:43
@article{5dd7470b-b975-4a53-bb1b-283025ba3012,
abstract = {{<p>Aging and aging-related neurodegenerative disorders, such as Alzheimer’s disease, are characterized by chronic inflammation that progressively damages nervous tissue within the central nervous system (CNS). In addition to cytokines, lectin-like carbohydrate recognition molecules play a critical role in modifying cellular communication during inflammation. Among these, galectins—particularly anti-inflammatory galectin-1 and pro-inflammatory galectin-3—stand out due to their immunological functions and specificity for N-acetyllactosamine structures. Almost every cell type within the CNS can express and recognize galectins, influencing various essential cellular functions. N-acetyllactosamines, the ligand structures recognized by galectins, are found beneath sialylated termini in protein-linked oligosaccharides. During aging, protein-linked oligosaccharide structures become shorter, exposing N-acetyllactosamines on protein surfaces, which enhances their availability as binding sites for galectins. Genomic studies indicate that the number of galectin-1- and galectin-3-expressing microglial cells increases with age- or age-related disease (Alzheimer’s disease), reflecting an aging-associated rise in galectin concentrations within the CNS. This increase parallels a rise in free N-acetyllactosamine-like ligands, suggesting that galectin-N-acetyllactosamine interactions gain prominence and play a more significant role in aging-related CNS disorders. Understanding these interactions and their molecular implications offers potential avenues for targeted therapeutic strategies in combating aging-related CNS inflammation and neurodegeneration.</p>}},
author = {{Mir, Mohd Yaqub and Legradi, Adam}},
issn = {{1661-6596}},
keywords = {{aging; galectins; glycan–lectin interaction; neuroinflammation}},
language = {{eng}},
number = {{10}},
publisher = {{MDPI AG}},
series = {{International Journal of Molecular Sciences}},
title = {{Sweet Aging : Glycocalyx and Galectins in CNS Aging and Neurodegenerative Disorders}},
url = {{http://dx.doi.org/10.3390/ijms26104699}},
doi = {{10.3390/ijms26104699}},
volume = {{26}},
year = {{2025}},
}