Table 1.
Glycoprotein | Significance | PTM | Disease(s) and associated pathologies |
Underlying mechanism |
Potential therapeutic modalities |
Research model(s) |
Reference (s) |
---|---|---|---|---|---|---|---|
Lectin targets (galectin, siglec) |
Development, axonal tracing and neurite fasciculation |
N-acetyllactosamine | Impaired repair and regeneration.Liver cirrhosis.Heart failure.Neoplastic transformation |
Upregulation of lectins | Galectin-3 inhibitor; TD139 | RatMouseSTEM cells |
53,58 |
Neural cell adhesion molecules (neuroserpin) |
Neurogenesis | Polysialic acid and N-glycosylation |
Alzheimer’s diseaseCancer (myeloma, myeloid leukemia, lymphoma, and others) |
Signaling through axon guidance receptors (EphA2, neuropilin-1, Robo, and DCC) |
Radioimmunolocalization of metastases using NCAM-binding radioim- munoconjugates |
RatCells | 142,143 |
β-Amyloid | Pro-inflammatory and cholesterol regulation |
Bisecting N-GlcNAc | Alzheimer’s dis- ease.Dementia.Amyloid angiopathy |
Increase in N-acetylglucosaminyltransferase III (GnT-III) producingβ-amyloid that causes oxidative stress, lipid peroxidation and mitochondrial impairment |
Upregulation of the expression of bisecting N-glycans |
Mouse | 93 |
Tau | Cytoskeletal stabilization |
N-glycosylation and hyperphosphoryla- tion |
Alzheimer’s disease.Parkinson’s dis- ease.Dementia.Traumatic brain injury |
Defective tau weakly stabilizes cytoskeletal microtubules.Tau activity decreases with age |
New treatment with curcumin is under investigation.Early detection by associated biomarkers |
Saliva samples | [144] |
Transferrin (ceruloplasmin) |
Iron homeostasis | N-glycosylation | Alzheimer’s disease.Parkinson’s disease.Iron overload anemia.Protein malnutrition |
Abnormal binding to available iron | Targeting transferrin (Trf) and its receptor |
CSF samples | 145 |
Neuronal pentraxin | Pattern recognition receptor; acute immune response and neuronal plasticity |
N-glycosylation | Parkinson’s disease | Immune response and acute inflammation, acute phase proteins |
Goeckerman’s therapy (GT) |
Human SN and frontal cortex |
104 |
Nicastrin | Part of the complex that cleaves APP |
O-GlcNAcylated | Alzheimer’s disease | Reduction of γ-secretase activity and Aβ production |
Antinicastrin antibodies | CSF samples | 90 |
α-Synuclein | Synaptic maintenance | O-glycosylation | Parkinson’s dis- ease.Dememtia.System atro- phy.Synucleinopathies |
Interacts with tubulin as a potential microtubule-associated protein |
Inhibit aggregation of α-synuclein-like cuminaldehyde |
MouseCells | 140 |
Biglycan | Antoi-apototic | Glycosaminoglycan- like glycosylation |
Alzheimer’s disease.Parkinson’s disease.Amyotrophic lateral sclerosis.Multiple sclerosis.Huntington’s disease |
NF-κB mediated NO-induced apoptotic cell death |
Biglycan gene therapy | Cells | 148 |
Acetylcholinesterase (also butyryl- cholinesterase) |
Cleaves Ach | Amphiphilic dimeric and monomeric AChE isoforms |
Alzheimer’s disease (AChE is almost specific).Muscular paralysis and convulsions |
Increased Ach in the frontal cortex.Increase in amyloidStress and inflammation |
Pharmacological intervention |
CSF samples | 89 |
PP2A | Major brain tau phosphatase |
Methylation and glycosylation |
Parkinson’s disease.Alzheimer’s disease.Traumatic brain injury.Cancer |
Reduce tau hyperphosphorylation | PP2 as a biological target but recent evidence suggest its role as a tumor suppressor protein |
Rat | 149 |