Lipids at the Nexus between Cerebrovascular Disease and Vascular Dementia: The Impact of HDL-Cholesterol and Ceramides

Sergi, Domenico; Zauli, Enrico; Tisato, Veronica; Secchiero, Paola; Zauli, Giorgio; Cervellati, Carlo

doi:10.3390/ijms24054403

Cited by 12 publications

(5 citation statements)

References 162 publications

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“…Earlier we noted that vascular dementia is also linked to infection (35). Vascular dementia has similar characteristics to AD, PD, and LBD: the arteries contain plaque, and the epithelial cell lining of the arteries, veins, and capillaries are pigmented with melanin (91,92), which we theorize provides energy. We suggest researchers determine if the epithelial cells of individuals with vascular dementia have reduced melanin levels in the vasculature of their brains and/or heart or in the area of a deep vein thrombosis or other cardiac event that may have occurred, increased lipids, and mitochondrial dysfunction.…”

Section: Electrical Charge and Electromagnetic Synthesismentioning

confidence: 81%

Melanin: a unifying theory of disease as exemplified by Parkinson’s, Alzheimer’s, and Lewy body dementia

Berg,

Berg

2023

Front. Immunol.

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Melanin, a ubiquitous dark pigment, plays important roles in the immune system, including scavenging reactive oxygen species formed in response to ultraviolet radiation absorption, absorbing metals, thermal regulation, drug uptake, innate immune system functions, redox, and energy transduction. Many tissue types, including brain, heart, arteries, ovaries, and others, contain melanin. Almost all cells contain precursors to melanin. A growing number of diseases in which there is a loss of melanin and/or neuromelanin are increasingly thought to have infectious etiologies, for example, Alzheimer’s disease (AD), Parkinson’s disease (PD), Lewy Body Dementia (LBD), and vitiligo. AD, PD, LBD, and vitiligo have been linked with herpesvirus, which enters melanosomes and causes apoptosis, and with gut dysbiosis and inflammation. Herpesvirus is also linked with gut dysbiosis and inflammation. We theorize that under normal healthy states, melanin retains some of the energy it absorbs from electromagnetic radiation, which is then used to fuel cells, and energy from ATP is used to compliment that energy supply. We further theorize that loss of melanin reduces the energy supply of cells, which in the case of AD, PD, and LBD results in an inability to sustain immune system defenses and remove the plaques associated with the disease, which appear to be part of the immune system’s attempt to eradicate the pathogens seen in these neurodegenerative diseases. In addition, in an attempt to explain why removing these plaques does not result in improvements in cognition and mood and why cognitions and moods in these individuals have ebbs and flows, we postulate that it is not the plaques that cause the cognitive symptoms but, rather, inflammation in the brain resulting from the immune system's response to pathogens. Our theory that energy retained in melanin fuels cells in an inverse relationship with ATP is supported by studies showing alterations in ATP production in relationship to melanin levels in melanomas, vitiligo, and healthy cells. Therefore, alteration of melanin levels may be at the core of many diseases. We propose regulating melanin levels may offer new avenues for treatment development.

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Section: Electrical Charge and Electromagnetic Synthesismentioning

confidence: 81%

Melanin: a unifying theory of disease as exemplified by Parkinson’s, Alzheimer’s, and Lewy body dementia

Berg,

Berg

2023

Front. Immunol.

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“…Thus, the impact of HDL-cholesterol on cardiovascular health is not only dictated by its circulating levels, but also by the functionality of HDL particles, namely, their antioxidant, anti-inflammatory, and cholesterol efflux capacity, which are crucial for HDL lipoproteins to elicit their cardioprotective effects [8,9]. In line with this, an impairment in HDL-antioxidant, anti-inflammatory, and cholesterol efflux capacity is intimately linked with CVD [10][11][12][13][14][15]. In addition to HDL functionality, HDL-cholesterol distribution is also emerging as an important player in dictating the effect of HDL lipoproteins on cardiovascular health [16,17].…”

Section: Introductionmentioning

confidence: 94%

HDL-Cholesterol Subfraction Dimensional Distribution Is Associated with Cardiovascular Disease Risk and Is Predicted by Visceral Adiposity and Dietary Lipid Intake in Women

Sergi,

Sanz,

Trentini

et al. 2024

Nutrients

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HDL-cholesterol quality, including cholesterol distribution in HDL subfractions, is emerging as a key discriminant in dictating the effects of these lipoproteins on cardiovascular health. This study aims at elucidating the relationship between cholesterol distribution in HDL subfractions and CVD risk factors as well as diet quality and energy density in a population of pre- and postmenopausal women. Seventy-two women aged 52 ± 6 years were characterized metabolically and anthropometrically. Serum HDL-C subfractions were quantified using the Lipoprint HDL System. Cholesterol distribution in large HDL subfractions was lower in overweight individuals and study participants with moderate to high estimated CVD risk, hypertension, or insulin resistance. Cholesterol distribution in large, as opposed to small, HDL subfractions correlated negatively with insulin resistance, circulating triglycerides, and visceral adipose tissue (VAT). VAT was an independent positive and negative predictor of cholesterol distribution in large and small HDL subfractions, respectively. Furthermore, an increase in energy intake could predict a decrease in cholesterol levels in large HDL subfractions while lipid intake positively predicted cholesterol levels in small HDL subfractions. Cholesterol distribution in HDL subfractions may represent an additional player in shaping CVD risk and a novel potential mediator of the effect of diet on cardiovascular health.

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“…Studies have shown that calcium channel genes, autonomic nervous system abnormalities (increased norepinephrine) and increased cortisol are all associated with MVD and depression in hypertensive patients ( 45 , 46 , 48 ). Depressed patients frequently exhibit low levels of high-density lipoprotein cholesterol (HDL-C) and elevated triglyceride levels, both of which promote the growth of atherosclerosis, which is a key driver of vascular disease ( 49 ). In addition, autonomic nervous dysfunction and neurohormone imbalance, inflammatory reaction and hippocampal structural alterations are all significant factors that contribute to the complex and bidirectional association between DM and depression ( 40 , 50 ).…”

Section: Risk Factorsmentioning

confidence: 99%

Association between depression and macrovascular disease: a mini review

2023

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Depression and macrovascular diseases are globally recognized as significant disorders that pose a substantial socioeconomic burden because of their associated disability and mortality. In addition, comorbidities between depression and macrovascular diseases have been widely reported in clinical settings. Patients afflicted with coronary artery disease, cerebrovascular disease or peripheral artery disease exhibit an elevated propensity for depressive symptoms. These symptoms, in turn, augment the risk of macrovascular diseases, thereby reflecting a bidirectional relationship. This review examines the physiological and pathological mechanisms behind comorbidity while also examining the intricate connection between depression and macrovascular diseases. The present mechanisms are significantly impacted by atypical activity in the hypothalamic–pituitary–adrenal axis. Elevated levels of cortisol and other hormones may disrupt normal endothelial cell function, resulting in vascular narrowing. At the same time, proinflammatory cytokines like interleukin-1 and C-reactive protein have been shown to disrupt the normal function of neurons and microglia by affecting blood–brain barrier permeability in the brain, exacerbating depressive symptoms. In addition, platelet hyperactivation or aggregation, endothelial dysfunction, and autonomic nervous system dysfunction are important comorbidity mechanisms. Collectively, these mechanisms provide a plausible physiological basis for the interplay between these two diseases. Interdisciplinary collaboration is crucial for future research aiming to reveal the pathogenesis of comorbidity and develop customised prevention and treatment strategies.

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Lipids at the Nexus between Cerebrovascular Disease and Vascular Dementia: The Impact of HDL-Cholesterol and Ceramides

Cited by 12 publications

References 162 publications

Melanin: a unifying theory of disease as exemplified by Parkinson’s, Alzheimer’s, and Lewy body dementia

Melanin: a unifying theory of disease as exemplified by Parkinson’s, Alzheimer’s, and Lewy body dementia

HDL-Cholesterol Subfraction Dimensional Distribution Is Associated with Cardiovascular Disease Risk and Is Predicted by Visceral Adiposity and Dietary Lipid Intake in Women

Association between depression and macrovascular disease: a mini review

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