Common Aging Signature in the Peripheral Blood of Vascular Dementia and Alzheimer’s Disease

2015 ◽  
Vol 53 (6) ◽  
pp. 3596-3605 ◽  
Author(s):  
Hongbo Luo ◽  
Guangchun Han ◽  
Jiajia Wang ◽  
Fan Zeng ◽  
Yuanming Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Peripheral Blood

scholarly journals Serum adiponectin and methylation of adiponectin gene promoter in peripheral blood of the patients with Alzheimer’s disease and vascular dementia

2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Aiym Kaiyrlykyzy ◽  
Andrey Tsoy ◽  
Bauyrzhan Umbayev ◽  
Farkhad Olzhayev ◽  
Dinara Alzhanova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia ◽  
Peripheral Blood ◽  
Gene Promoter ◽  
Serum Adiponectin ◽  
Adiponectin Gene

Assessment of the severity of endogenous intoxication in Alzheimer's disease

2020 ◽  
Vol 63 (7) ◽  
pp. 119-125
Author(s):  
Maria G. Engalycheva ◽  
◽  
Maria A. Fomina ◽  
Dmitry S. Petrov ◽  
Daria I. Miroshnikova ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Molecular Weight ◽  
Nucleic Acids ◽  
Vascular Dementia ◽  
Peripheral Blood ◽  
Oxidative Modification ◽  
Mononuclear Leukocytes ◽  
Endogenous Intoxication ◽  
Radical Processes

The development of neurodegenerative pathologies, among which the leading positions worldwide belong to Alzheimer's disease, is accompanied by the activation of free radical processes in the tissues of the brain and in the patient's body as a whole, which leads to the accumulation of products of oxidative modification of proteins, lipids, nucleic acids, and the formation of a syndrome of endogenous intoxication. An integral indicator reflecting the severity of this syndrome is the level of substances of low and medium molecular weight in various biological media. It is known that changes at the molecular level in Alzheimer's disease occur 5-10 years before the clinical manifestation of pathology. The development of polymodal panels for biochemical screening, diagnostics, monitoring of the course of pathology is underway. The aim of this study was to determine the severity of endogenous intoxication in patients with Alzheimer's disease and vascular dementia. The object of the study was the blood plasma of patients, as well as fractionated leukocytes - mononuclear and polymorphonuclear. The choice of biological material for the study is dictated by the need to search for a prognostic marker of the disease available for diagnosis, as well as by the accumulated theoretical material on various metabolic changes in peripheral blood cells in neurodegenerative diseases. According to the results of the study, it was found that in patients with Alzheimer's disease in mononuclear leukocytes of peripheral blood, the level of substances of low and medium molecular weight is higher than in patients with vascular dementia and patients without signs of neurodegeneration. In addition, in this fraction of leukocytes, the concentration of hypoxanthine, inosine, xanthosine and their derivatives is high, which may be a consequence of the oxidative modification of nucleic acids in the cells under study.

SPECIFIC PROPERTIES OF TUBULIN IN THE PREFRONTAL CORTEX IN CONTROL, SCHIZOPHRENIA AND VASCULAR DEMENTIA

2020 ◽  
pp. 65-71
Author(s):  
Burbaeva G.Sh. ◽  
Androsova L.V. ◽  
Vorobyeva E.A. ◽  
Savushkina O.K.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Prefrontal Cortex ◽  
Vascular Dementia ◽  
Binding Activity ◽  
Nephelometric Method ◽  
Rate Of Polymerization ◽  
Mental Diseases ◽  
And Control ◽  
The Brain

The aim of the study was to evaluate the rate of polymerization of tubulin into microtubules and determine the level of colchicine binding (colchicine-binding activity of tubulin) in the prefrontal cortex in schizophrenia, vascular dementia (VD) and control. Colchicine-binding activity of tubulin was determined by Sherlinе in tubulin-enriched extracts of proteins from the samples. Measurement of light scattering during the polymerization of the tubulin was carried out using the nephelometric method at a wavelength of 450-550 nm. There was a significant decrease in colchicine-binding activity and the rate of tubulin polymerization in the prefrontal cortex in both diseases, and in VD to a greater extent than in schizophrenia. The obtained results suggest that not only in Alzheimer's disease, but also in other mental diseases such as schizophrenia and VD, there is a decrease in the level of tubulin in the prefrontal cortex of the brain, although to a lesser extent than in Alzheimer's disease, and consequently the amount of microtubules.

Recent Updates on the Association Between Alzheimer's Disease and Vascular Dementia

2016 ◽  
Vol 12 (3) ◽  
pp. 226-237 ◽  
Author(s):  
Ghulam M. Ashraf ◽  
Sandesh Chibber ◽  
. Mohammad ◽  
Syed K. Zaidi ◽  
Shams Tabrez ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Vascular Dementia

scholarly journals Association between methylation of BIN1 promoter in peripheral blood and preclinical Alzheimer’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Hao Hu ◽  
Lan Tan ◽  
Yan-Lin Bi ◽  
Wei Xu ◽  
Lin Tan ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Peripheral Blood ◽  
Late Onset ◽  
Early Stage ◽  
Susceptibility Gene ◽  
Subjective Cognitive Decline ◽  
Preclinical Ad ◽  
T Tau ◽  
New Evidence

AbstractThe bridging integrator 1 (BIN1) gene is the second most important susceptibility gene for late-onset Alzheimer’s disease (LOAD) after apolipoprotein E (APOE) gene. To explore whether the BIN1 methylation in peripheral blood changed in the early stage of LOAD, we included 814 participants (484 cognitively normal participants [CN] and 330 participants with subjective cognitive decline [SCD]) from the Chinese Alzheimer’s Biomarker and LifestylE (CABLE) database. Then we tested associations of methylation of BIN1 promoter in peripheral blood with the susceptibility for preclinical AD or early changes of cerebrospinal fluid (CSF) AD-related biomarkers. Results showed that SCD participants with significant AD biological characteristics had lower methylation levels of BIN1 promoter, even after correcting for covariates. Hypomethylation of BIN1 promoter were associated with decreased CSF Aβ42 (p = 0.0008), as well as increased p-tau/Aβ42 (p = 0.0001) and t-tau/Aβ42 (p < 0.0001) in total participants. Subgroup analysis showed that the above associations only remained in the SCD subgroup. In addition, hypomethylation of BIN1 promoter was also accompanied by increased CSF p-tau (p = 0.0028) and t-tau (p = 0.0130) in the SCD subgroup, which was independent of CSF Aβ42. Finally, above associations were still significant after correcting single nucleotide polymorphic sites (SNPs) and interaction of APOE ɛ4 status. Our study is the first to find a robust association between hypomethylation of BIN1 promoter in peripheral blood and preclinical AD. This provides new evidence for the involvement of BIN1 in AD, and may contribute to the discovery of new therapeutic targets for AD.

Sign in / Sign up

Export Citation Format

Share Document