Circulating Endothelial Progenitor Cells Reduce the Risk of Alzheimer’s Disease

Wang, Yixuan; Huang, Jinghan; Ang, Ting Fang Alvin; Zhu, Yibo; Qin, Tao; Mez, Jesse; Alosco, Michael L.; Denis, Gerald V.; Belkina, Anna C.; Gurnani, Ashita S.; Ross, Mark; Gong, Bin; Han, Jing‐Yan; Lunetta, Kathryn L.; Stein, Thor D.; Au, Rhoda; Farrer, Lindsay A.; Qiu, Wei Qiao

doi:10.1101/2023.01.16.23284571

Cited by 2 publications

(2 citation statements)

References 74 publications

(89 reference statements)

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“…One of the most important criteria can be the level of EPCs: elevated numbers of EPCs with CD34+ and CD133+ co-expressions had a dose-dependent association with decreased AD risk. It is therefore tempting to suggest that all natural and therapeutic factors that elevate the level of EPCs can be therapeutic in reducing AD and related disease risks in the presence of cerebrovascular pathology [98]. Further investigation of the relationship between endothelial biomarkers and their dynamic with functional state and age-related diseases is warranted.…”

Section: Discussionmentioning

confidence: 99%

Immunological Profile and Markers of Endothelial Dysfunction in Elderly Patients with Cognitive Impairments

Goncharov,

Popova,

Kudryavtsev

et al. 2024

IJMS

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The process of aging is accompanied by a dynamic restructuring of the immune response, a phenomenon known as immunosenescence. Further, damage to the endothelium can be both a cause and a consequence of many diseases, especially in elderly people. The purpose of this study was to carry out immunological and biochemical profiling of elderly people with acute ischemic stroke (AIS), chronic cerebral circulation insufficiency (CCCI), prediabetes or newly diagnosed type II diabetes mellitus (DM), and subcortical ischemic vascular dementia (SIVD). Socio-demographic, lifestyle, and cognitive data were obtained. Biochemical, hematological, and immunological analyses were carried out, and extracellular vesicles (EVs) with endothelial CD markers were assessed. The greatest number of significant deviations from conditionally healthy donors (HDs) of the same age were registered in the SIVD group, a total of 20, of which 12 were specific and six were non-specific but with maximal differences (as compared to the other three groups) from the HDs group. The non-specific deviations were for the MOCA (Montreal Cognitive Impairment Scale), the MMSE (Mini Mental State Examination) and life satisfaction self-assessment scores, a decrease of albumin levels, and ADAMTS13 (a Disintegrin and Metalloproteinase with a Thrombospondin Type 1 motif, member 13) activity, and an increase of the VWF (von Willebrand factor) level. Considering the significant changes in immunological parameters (mostly Th17-like cells) and endothelial CD markers (CD144 and CD34), vascular repair was impaired to the greatest extent in the DM group. The AIS patients showed 12 significant deviations from the HD controls, including three specific to this group. These were high NEFAs (non-esterified fatty acids) and CD31 and CD147 markers of EVs. The lowest number of deviations were registered in the CCCI group, nine in total. There were significant changes from the HD controls with no specifics to this group, and just one non-specific with a maximal difference from the control parameters, which was α1-AGP (alpha 1 acid glycoprotein, orosomucoid). Besides the DM patients, impairments of vascular repair were also registered in the CCCI and AIS patients, with a complete absence of such in patients with dementia (SIVD group). On the other hand, microvascular damage seemed to be maximal in the latter group, considering the biochemical indicators VWF and ADAMTS13. In the DM patients, a maximum immune response was registered, mainly with Th17-like cells. In the CCCI group, the reaction was not as pronounced compared to other groups of patients, which may indicate the initial stages and/or compensatory nature of organic changes (remodeling). At the same time, immunological and biochemical deviations in SIVD patients indicated a persistent remodeling in microvessels, chronic inflammation, and a significant decrease in the anabolic function of the liver and other tissues. The data obtained support two interrelated assumptions. Taking into account the primary biochemical factors that trigger the pathological processes associated with vascular pathology and related diseases, the first assumption is that purine degradation in skeletal muscle may be a major factor in the production of uric acid, followed by its production by non-muscle cells, the main of which are endothelial cells. Another assumption is that therapeutic factors that increase the levels of endothelial progenitor cells may have a therapeutic effect in reducing the risk of cerebrovascular disease and related neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 99%

Immunological Profile and Markers of Endothelial Dysfunction in Elderly Patients with Cognitive Impairments

Goncharov,

Popova,

Kudryavtsev

et al. 2024

IJMS

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“…Human studies also indicate a role of ECFCs in NDDs, however with variable as well as contradictory results, reporting increased [274], unchanged [275,276], or decreased cell numbers [277,278], possibly due to limited cohort sizes. A new study with over 1500 subjects-currently only published as a preprint-shows a correlation between the number of circulating ECFCs and a reduced risk of AD [279].…”

Section: Endothelial Progenitor Cells In Neurodegenerative Disordersmentioning

confidence: 99%

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

Kulovic-Sissawo,

Tocantins,

Diniz

et al. 2024

Biology

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Endothelial dysfunction is associated with several lifestyle-related diseases, including cardiovascular and neurodegenerative diseases, and it contributes significantly to the global health burden. Recent research indicates a link between cardiovascular risk factors (CVRFs), excessive production of reactive oxygen species (ROS), mitochondrial impairment, and endothelial dysfunction. Circulating endothelial progenitor cells (EPCs) are recruited into the vessel wall to maintain appropriate endothelial function, repair, and angiogenesis. After attachment, EPCs differentiate into mature endothelial cells (ECs). Like ECs, EPCs are also susceptible to CVRFs, including metabolic dysfunction and chronic inflammation. Therefore, mitochondrial dysfunction of EPCs may have long-term effects on the function of the mature ECs into which EPCs differentiate, particularly in the presence of endothelial damage. However, a link between CVRFs and impaired mitochondrial function in EPCs has hardly been investigated. In this review, we aim to consolidate existing knowledge on the development of mitochondrial and endothelial dysfunction in the vascular endothelium, place it in the context of recent studies investigating the consequences of CVRFs on EPCs, and discuss the role of mitochondrial dysfunction. Thus, we aim to gain a comprehensive understanding of mechanisms involved in EPC deterioration in relation to CVRFs and address potential therapeutic interventions targeting mitochondrial health to promote endothelial function.

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Circulating Endothelial Progenitor Cells Reduce the Risk of Alzheimer’s Disease

Cited by 2 publications

References 74 publications

Immunological Profile and Markers of Endothelial Dysfunction in Elderly Patients with Cognitive Impairments

Immunological Profile and Markers of Endothelial Dysfunction in Elderly Patients with Cognitive Impairments

Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells

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