Evaluation of serum galectin-3 levels at Alzheimer patients by stages: a preliminary report

Yazar, Tamer; Yazar, Hülya Olgun; Cihan, Murat

doi:10.1007/s13760-020-01477-1

Cited by 24 publications

(19 citation statements)

References 44 publications

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“…Gal-3 is involved in several relevant biological processes exerting pleiotropic functions that include: cell adhesion, proliferation, migration, apoptosis, and inflammation (Dong et al, 2018;Tan et al, 2021). Gal-3 is increased in the serum of AD patients (Yazar et al, 2020), as well as it is ten folds increased in microglia of AD brains and 5XFAD mice (Boza-Serrano et al, 2019). Plaque-associated microglia are the predominant cell type expressing Gal-3 in humans and mice.…”

Section: Microglia In Alzheimer's Diseasementioning

confidence: 99%

Microglia in Neuroinflammation and Neurodegeneration: From Understanding to Therapy

2021

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Microglia are the resident macrophages of the central nervous system (CNS) acting as the first line of defense in the brain by phagocytosing harmful pathogens and cellular debris. Microglia emerge from early erythromyeloid progenitors of the yolk sac and enter the developing brain before the establishment of a fully mature blood–brain barrier. In physiological conditions, during brain development, microglia contribute to CNS homeostasis by supporting cell proliferation of neural precursors. In post-natal life, such cells contribute to preserving the integrity of neuronal circuits by sculpting synapses. After a CNS injury, microglia change their morphology and down-regulate those genes supporting homeostatic functions. However, it is still unclear whether such changes are accompanied by molecular and functional modifications that might contribute to the pathological process. While comprehensive transcriptome analyses at the single-cell level have identified specific gene perturbations occurring in the “pathological” microglia, still the precise protective/detrimental role of microglia in neurological disorders is far from being fully elucidated. In this review, the results so far obtained regarding the role of microglia in neurodegenerative disorders will be discussed. There is solid and sound evidence suggesting that regulating microglia functions during disease pathology might represent a strategy to develop future therapies aimed at counteracting brain degeneration in multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis.

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Section: Microglia In Alzheimer's Diseasementioning

confidence: 99%

Microglia in Neuroinflammation and Neurodegeneration: From Understanding to Therapy

2021

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“…Amongst molecules implicated in Alzheimer's disease (AD), Gal-3 has recently emerged as one of the most promising, mechanistically and therapeutically [6,173]. Gal-3 concentrations are increased in the brains, CSF and plasma of humans with AD [174][175][176] and Gal-3 brain injections increase insoluble Aβ levels and toxicity in animals [11,177]. Endogenous Gal-3 is most highly expressed in Aβ plaques [11].…”

Section: Gal-3 Elicits Alzheimer's Pathology and Symptomsmentioning

confidence: 99%

Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases

Soares

Al‐Dalahmah

Hillis

et al. 2021

Cells

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Galectin-3 (Gal-3) is an evolutionarily conserved and multifunctional protein that drives inflammation in disease. Gal-3’s role in the central nervous system has been less studied than in the immune system. However, recent studies show it exacerbates Alzheimer’s disease and is upregulated in a large variety of brain injuries, while loss of Gal-3 function can diminish symptoms of neurodegenerative diseases such as Alzheimer’s. Several novel molecular pathways for Gal-3 were recently uncovered. It is a natural ligand for TREM2 (triggering receptor expressed on myeloid cells), TLR4 (Toll-like receptor 4), and IR (insulin receptor). Gal-3 regulates a number of pathways including stimulation of bone morphogenetic protein (BMP) signaling and modulating Wnt signalling in a context-dependent manner. Gal-3 typically acts in pathology but is now known to affect subventricular zone (SVZ) neurogenesis and gliogenesis in the healthy brain. Despite its myriad interactors, Gal-3 has surprisingly specific and important functions in regulating SVZ neurogenesis in disease. Gal-1, a similar lectin often co-expressed with Gal-3, also has profound effects on brain pathology and adult neurogenesis. Remarkably, Gal-3’s carbohydrate recognition domain bears structural similarity to the SARS-CoV-2 virus spike protein necessary for cell entry. Gal-3 can be targeted pharmacologically and is a valid target for several diseases involving brain inflammation. The wealth of molecular pathways now known further suggest its modulation could be therapeutically useful.

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“…Another clinical study further found that the expression of galactin-3 in the frontal lobe was increased in patients with AD, while Aβ oligomerization was enhanced [90]. Furthermore, serum Gal-3 levels significantly paralleled the severity of memory loss [90] and the stage of AD [91].…”

Section: Gal-3 Levels Increased In Admentioning

confidence: 88%

“…The plasma Gal-3 levels have been detected by ELISAs (enzyme-linked immunosorbent assays) in the majority of relevant clinical studies [11,91]. This approach is simple and accessible for clinical practice.…”

Section: Gal-3 As a Biomarkermentioning

confidence: 99%

Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

Tan

Zheng

et al. 2021

Cell Biosci

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Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the deposition of extracellular aggregates of amyloid-β (Aβ), the formation of intraneuronal tau neurofibrillary tangles and microglial activation-mediated neuroinflammation. One of the key molecules involved in microglial activation is galectin-3 (Gal-3). In recent years, extensive studies have dissected the mechanisms by which Gal-3 modulates microglial activation, impacting Aβ deposition, in both animal models and human studies. In this review article, we focus on the emerging role of Gal-3 in biology and pathobiology, including its origin, its functions in regulating microglial activation and neuroinflammation, and its emergence as a biomarker in AD and other neurodegenerative diseases. These aspects are important to elucidate the involvement of Gal-3 in AD pathogenesis and may provide novel insights into the use of Gal-3 for AD diagnosis and therapy.

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Evaluation of serum galectin-3 levels at Alzheimer patients by stages: a preliminary report

Cited by 24 publications

References 44 publications

Microglia in Neuroinflammation and Neurodegeneration: From Understanding to Therapy

Microglia in Neuroinflammation and Neurodegeneration: From Understanding to Therapy

Novel Galectin-3 Roles in Neurogenesis, Inflammation and Neurological Diseases

Galectin-3: a key player in microglia-mediated neuroinflammation and Alzheimer's disease

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