BACKGROUND: Atherosclerosis is considered a crucial component in the pathogenesis of decreased cognitive function, as occurs in vascular cognitive impairment (VCI). Inflammation and the immune response play a significant role in the development of many chronic diseases. Immunoglobulin G (IgG) N-glycosylation has been implicated in the development of a variety of diseases by affecting the anti-inflammatory and proinflammatory responses of IgG. This study aimed to investigate the association between IgG N-glycosylation and VCI in a sample of patients with atherosclerosis through a case-control study.
METHODS: We recruited a total of 330 patients with atherosclerosis to participate in this case-control study, including 165 VCI patients and 165 sex- and age-matched participants with normal cognitive function. The plasma IgG N-glycans of participants were separated by ultrahigh-performance liquid chromatography. An enzyme-linked immunosorbent assay (ELISA) kit was used to determine the corresponding serum inflammatory factors. Atherosclerosis was diagnosed by carotid ultrasound, and the diagnosis of VCI was based on the \"Guidelines for the Diagnosis and Treatment of Vascular Cognitive Impairment in China (2019)\". A multivariate logistic regression model was used to explore the association between IgG N-glycans and VCI. We also analyzed the relationship between IgG N-glycans and the inflammatory state of VCI through canonical correlation analysis (CCA).
RESULTS: Through the multivariate logistic regression analysis, 8 glycans and 13 derived traits reflecting decreased sialylation and galactosylation and increased bisecting GlcNAc significantly differed between the case and control groups after adjusting for confounding factors (P < 0.05, q < 0.05). Similarly, the differences in TNF-α, IL-6, and IL-10 were statistically significant between the case and control groups after adjusting for the effects of confounding factors (P < 0.05, q < 0.05). The CCA results showed that VCI-related initial N-glycans were significantly correlated with VCI-related inflammatory factors (r = 0.272, P = 0.004). The combined AUC value (AUC combined = 0.885) of 7 initial glycans and inflammatory factors was higher than their respective values (AUC initial glycans = 0.818, AUC inflammatory factors = 0.773).
CONCLUSIONS: The findings indicate that decreased sialylation and galactosylation and increased bisecting GlcNAc reflected by IgG N-glycans might affect the occurrence of VCI in patients with atherosclerosis though promoting the proinflammatory function of IgG. IgG N-glycans may serve as potential biomarkers to distinguish VCI in individuals with atherosclerosis.

Vascular Parkinsonism (VP) is a form of secondary Parkinsonism resulting from cerebrovascular disease. Estimates of the frequency of VP vary greatly worldwide; 3% to 6% of all cases of Parkinsonism are found to have a vascular etiology. In a Brazilian community-based study on Parkinsonism, 15.1% of all cases were classified as VP, the third most common form, with a prevalence of 1.1% in an elderly cohort. Another Brazilian survey found a prevalence of 2.3% of VP in the elderly. VP is usually the result of conventional vascular risk factors, particularly hypertension, leading to strategic infarcts of subcortical gray matter nuclei, diffuse white matter ischaemic lesions and less commonly, large vessel infarcts. Patients with VP tend to be older and present with gait difficulties, symmetrical predominant lower-body involvement, poor levodopa responsiveness, postural instability, falls, cognitive impairment and dementia, corticospinal findings, urinary incontinence and pseudobulbar palsy. This article intends to provide physicians with an insight on the practical issues of VP, a disease potentially confounded with vascular dementia, idiopathic Parkinson\'s disease, dementia with Lewy bodies and other secondary causes of Parkinsonism.
Parkinsonismo vascular (VP) é a forma secundária da síndrome parkinsoniana resultante de doença cerebrovascular. Há grande variação das estimativas de frequência em estudos mundiais, sendo que em média 3% a 6% de todos os casos de parkinsonismo têm a etiologia vascular. Em um estudo brasileiro de base comunitária sobre parkinsonismo, 15,1% de todos os casos foram classificados como VP, que foi a terceira causa mais comum, com uma prevalência de 1,1% em uma coorte de idosos. Outro estudo brasileiro encontrou uma prevalência de 2,3% de VP também em idosos. VP usualmente resulta de fatores de risco vasculares como a hipertensão, levando a infartos estratégicos nos núcleos da base, lesões isquêmicas difusas da substância branca subcortical e menos comumente, infartos de grandes vasos. Os pacientes com VP geralmente são mais idosos e apresentam dificuldades para a marcha, envolvimento simétrico predominante em membros inferiores, resposta pobre à terapêutica com levodopa, instabilidade postural e quedas, comprometimento cognitivo e demência, sinais de acometimento corticoespinhal, incontinência urinária e paralisia pseudobulbar. Este artigo apresenta algumas informações práticas sobre o VP, uma condição neurológica potencialmente confundida com demência vascular, doença de Parkinson idiopática, demência com corpos de Lewy e com outras causas de parkinsonismo.