Table 1 Brief summary of clinical studies on the concentration and role of Gal-3 in AD
From: Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease
Study population | Locations | Method | Main findings | Authors |
|---|---|---|---|---|
5804 participants aged 70–82 years were followed for 9–48 months | LGALS3 gene | MALDI-TOF MS | Genetic variation in the LGALS3 gene might be associated with cognitive function, and Gal-3 might influence cognitive function via the inflammatory response | Trompet et al. [88] |
41 AD patients and 46 healthy subjects (controls) | Serum Gal-3 levels | ELISA | Patients with AD presented higher Gal-3 levels than healthy controls. Serum Gal-3 could be a potential a biomarker for AD diagnosis | Wang et al. [11] |
31 AD patients and 50 healthy subjects (controls) | CSF and serum Gal-3 levels | ELISA | Serum and CSF galectin -3 levels in AD patients were higher than those in healthy controls. Serum Gal-3 concentration was positively correlated with the MMSE score | Ashraf et al. [89] |
57 AD patients and 61 healthy subjects (controls) | Serum Gal-3 levels | ELISA | Serum galactin-3 levels might be positively correlated with the stage of AD and be a potential biomarker for the identification of AD | Yazar et al. [91] |
4 AD patients and 4 healthy subjects (controls) | Frontal lobe tissue Gal-3 levels | Immunohistochemistry and western blot | Galactin-3 expression in the frontal lobe was increased in AD patients and paralleled Aβ oligomerization. Immunohistochemical results revealed colocalization of galactin-3 and amyloid plaques | Tao et al. [90] |
6 AD patients and 5 healthy subjects (controls) | Cortex tissue Gal-3 levels | Immunohistochemistry and western blot | Gal-3 was increased in AD patient brains and colocalized with microglia associated with Aβ plaques | Boza-Serrano et al. [12] |