Abstract
Alzheimer’s disease is a neurodegenerative disorder whose pathological mechanisms, despite recent advances, are not fully understood. However, the deposition of beta amyloid -peptide and neuroinflammation, which is probably aggravated by dysbiotic microbiota, seem to play a key role. Anti-Gal are the most abundant xenoreactive natural antibodies. They are supposed to stem from immunization against the gut microbiota and have been implicated in the pathogenesis of several diseases, including multiple sclerosis. These antibodies target the alpha-Gal epitope, expressed on the terminal sugar units of glycoprotein or glycolipid of all mammals except apes, Old World monkeys and humans. The alpha-Gal is constitutively expressed in several bacteria constituting the brain microbiota, and alpha-Gal-like epitopes have been detected in gray matter, amyloid plaque, neurofibrillary tangles and corpora amylacea of the human brain, suggesting a potential link between anti-Gal and Alzheimer’s disease etiopathogenesis. For the first time, our study searched for possible alterations of anti-Gal immunoglobulin levels in Alzheimer’s disease patients. IgG and IgM blood levels were significantly lower, and IgA significantly higher in patients than in healthy subjects. These results suggest that such immunoglobulins might be implicated in Alzheimer’s disease pathogenesis and open new scenarios in the research for new biomarkers and therapeutic strategies.
Highlights
Alzheimer’s disease (AD), the most common form of dementia, is a progressive, irreversible and incurable neurodegenerative disease, which constitutes one of the major causes of dependency, disability and mortality [1]
This study demonstrated that anti-Gal IgG and IgM were significantly decreased, and
IgA significantly increased in AD patients compared to healthy subjects (HS)
Summary
Alzheimer’s disease (AD), the most common form of dementia, is a progressive, irreversible and incurable neurodegenerative disease, which constitutes one of the major causes of dependency, disability and mortality [1]. There are over 50 million people worldwide living with dementia in 2020. This number will almost double every 20 years, reaching 82 million in 2030 and 152 million in 2050. Neurodegeneration is most likely caused by an abnormal accumulation of the beta amyloid peptide which produces a cascade of events, including an inflammatory process mainly mediated by microglial activation and formation of neurofibrillary tangles that culminate in neuronal death. The triggering mechanism of this cascade is still unknown and biomarkers with possible mechanistic insights into the AD pathophysiologic processes are urgently needed [3]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
