Antibodies Against Gangliosides in Patients With Dementia

Abstract

This study indicates that elevated IgM anti-GM1 may be connected with the neurodegeneration in older patients with severe dementia and that AD may also be associated with increased IgM anti-GD1b levels.

Primary Sjögren's syndrome is associated with significant cognitive dysfunction

“…In SS, antiganglioside antibodies were associated with evidence of neuropathy . Furthermore, antiganglioside antibodies may be related to dementia . In our study, patients with PSS had significantly higher rate of seropositivity for antiganglioside antibodies compared to controls.…”

“…Anti‐phospholipid antibodies, anti‐N‐methyl‐D‐aspartate (NMDA) receptor and anti‐ribosomal‐p autobodies in SLE and anti‐thyroid antibodies in Hashimoto's ensephalopathy have been reported . Moreover, antiganglioside antibodies may have a potential role in neurological manifestations of several diseases, such as neurodegenerative diseases, dementia, SLE, SS, mixed cryoglobulinemia and idiopathic systemic vasculitis . Likewise, antiganglioside antibodies are related to cognitive dysfunction in pediatric neuropsychiatric SLE .…”

High Levels of Anti-Ganglioside Antibodies in Patients with Parkinson?s Disease Associated with Cognitive Decline

“…Gangliosides' binding induces Aβ peptide oligomerization. GM1 and GT1b have four sugar moieties in common, however, GT1b has three sialic molecules more compared to asialo-GM1 that doesn't contain sialic rests [60].…”

“…In more recent reports Mandal et al demonstrated with NMR studies, the interaction of membrane-bound α-synuclein with Aβ. The presence of multiple sites of interaction between α-synuclein and Aβ might be important in determining the overlapping patho-cascades of AD and PD seen in DLB [60]. Preventing the interaction of membrane-bound α-synuclein with Aβ peptide would be an important therapeutic research target.…”

“…Asialo-GM1 and GM1 are able to bind Aβ and prevent by this binding the β-sheet formation [58]. Therefore, the loss of 'protective' GM1 and the increase of 'unprotective' GT1b during the senility, elevates the possibility of β-sheet formation and the resulting senile plaques [60][61][62]. Parkinson's disease concerns the degeneration of dopaminergic neurons of SubstantiaNigra, caused by genetic, neurotoxic and several other factors, that induce oxidative damage and cell death.…”