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Keywords = diabetic vascular dementia

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10 pages, 958 KiB  
Article
Minimally Invasive Surgery Versus Conventional Neurosurgical Treatments for Patients with Subcortical Supratentorial Intracerebral Hemorrhage: A Nationwide Study of Real-World Data from 2016 to 2022
by Huanwen Chen, Matthew K. McIntyre, Mihir Khunte, Ajay Malhotra, Mohamed Labib, Marco Colasurdo and Dheeraj Gandhi
Diagnostics 2025, 15(11), 1308; https://doi.org/10.3390/diagnostics15111308 - 23 May 2025
Viewed by 602
Abstract
Background: Neurosurgical interventions are often indicated for patients with subcortical, supratentorial intracerebral hemorrhage (ICH); however, the optimal treatment modality is controversial. Whether minimally invasive surgery (MIS) may be superior to conventional craniotomy (CC) or decompressive craniectomy (DC) in real-world clinical practice is [...] Read more.
Background: Neurosurgical interventions are often indicated for patients with subcortical, supratentorial intracerebral hemorrhage (ICH); however, the optimal treatment modality is controversial. Whether minimally invasive surgery (MIS) may be superior to conventional craniotomy (CC) or decompressive craniectomy (DC) in real-world clinical practice is unknown. Methods: This was a retrospective cohort study of hospitalization data from the 2016–22 Nationwide Readmissions Database. International Classification of Diseases—10th edition (ICD-10) codes were used to identify patients with primary supratentorial subcortical ICH who underwent neurosurgical treatment. Patients with ICH in other brain compartments (other than intraventricular hemorrhage) were excluded. Coprimary outcomes were routine discharge to home without rehabilitation needs (excellent outcome) and in-hospital mortality. Outcomes were compared between MIS versus CC and MIS versus DC, with multivariable adjustments for patient demographics and comorbidities. Results: A total of 3829 patients were identified; 418 underwent MIS (10.9%), 2167 (56.6%) underwent CC, and 1244 (32.5%) underwent DC. Compared to CC patients, MIS patients were less likely female (p = 0.004) but otherwise had similar patient characteristics; compared to DC patients, MIS patients were older, less likely female, more likely to have mental status abnormalities, more likely to have underlying dementia, less likely to undergo external ventricular drainage, more likely to have vascular risk factors (hypertension, hyperlipidemia, diabetes), and less likely to have underlying coagulopathy (all p < 0.05). After multivariable adjustments, MIS patients had higher odds of excellent outcomes compared to CC (OR 1.99 [95%CI 1.06–3.30], p = 0.039), and similar odds compared to DC (OR 1.10 [95%CI 0.66–1.86], p = 0.73). In terms of in-hospital mortality, MIS had lower odds compared to DC (OR 0.63 [95%CI 0.41–0.96], p = 0.032) and similar odds compared to CC (OR 0.81 [95%CI 0.56–1.18], p = 0.26). Conclusions: For patients with subcortical, supratentorial ICH requiring surgical evacuation, MIS was associated with higherhigher rates of excellent outcomes compared to CC and lower rates of in-hospital mortality compared to DC. However, since key variables such as hematoma size and symptom severity were not available, residual confounding could not be excluded, and results should be interpreted cautiously. Dedicated prospective or randomized studies are needed to confirm these findings. Full article
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8 pages, 351 KiB  
Brief Report
Screening for Post-Stroke Cognitive Impairment in Sub-Saharan Africa: A Good IDEA?
by Fode Abass Cissé, Yannick Fogoum Fogang, Male Dore and Gilles Naeije
Brain Sci. 2025, 15(6), 543; https://doi.org/10.3390/brainsci15060543 - 22 May 2025
Viewed by 482
Abstract
Background: Post-stroke cognitive impairment (PSCI) remains under-recognized in Sub-Saharan Africa (SSA), in part due to the lack of validated cognitive screening tools adapted to low-literacy populations. We aimed to validate the Identification of Dementia in Elderly Africans (IDEA) cognitive screen in SSA and [...] Read more.
Background: Post-stroke cognitive impairment (PSCI) remains under-recognized in Sub-Saharan Africa (SSA), in part due to the lack of validated cognitive screening tools adapted to low-literacy populations. We aimed to validate the Identification of Dementia in Elderly Africans (IDEA) cognitive screen in SSA and assess its utility for detecting PSCI in Guinea and Cameroon. Methods: Normative IDEA scores were derived from a control cohort of healthy older adults in Conakry (Guinea) and Bafoussam (Cameroon). The tool was then applied to consecutive stroke patients from the same hospitals within one month of stroke onset. Demographic, clinical, and vascular risk profiles were collected. Between-group comparisons were performed using Welch’s t-tests and chi-square tests. Results: Among 91 healthy controls (median age: 64), the mean IDEA score was 12 ± 2.4. A cut-off of ≤7 (2 standard deviations below the mean) was defined for cognitive impairment. Among 111 stroke patients (median age: 65; mean NIHSS: 9.9 ± 5.8), the mean IDEA score was 9.6 ± 3.2, and 31 patients (28%) had scores ≤ 7. Stroke patients had significantly higher rates of hypertension and diabetes compared to controls. Conclusions: The IDEA screen appears to be a feasible and effective tool for detecting PSCI in SSA clinical settings. The 28% prevalence of cognitive impairment aligns with data from high-income countries, supporting the broader use of the IDEA to strengthen cognitive care pathways in SSA stroke populations. Full article
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31 pages, 3560 KiB  
Review
The Promising Potency of Sodium–Glucose Cotransporter 2 Inhibitors in the Prevention of and as Treatment for Cognitive Impairment Among Type 2 Diabetes Patients
by Yibin Zhang, Xiaobin Liao, Jialu Xu, Jiaxin Yin, Shan Li, Mengni Li, Xiaoli Shi, Shujun Zhang, Chunyu Li, Weijie Xu, Xuefeng Yu and Yan Yang
Biomedicines 2024, 12(12), 2783; https://doi.org/10.3390/biomedicines12122783 - 6 Dec 2024
Cited by 1 | Viewed by 1497
Abstract
Type 2 diabetes mellitus (T2DM), accounting for the majority of diabetes mellitus prevalence, is associated with an increased risk of cognition decline and deterioration of cognition function in diabetic patients. The sodium–glucose cotransporter 2 (SGLT2), located in the renal proximal tubule, plays a [...] Read more.
Type 2 diabetes mellitus (T2DM), accounting for the majority of diabetes mellitus prevalence, is associated with an increased risk of cognition decline and deterioration of cognition function in diabetic patients. The sodium–glucose cotransporter 2 (SGLT2), located in the renal proximal tubule, plays a role in urine glucose reabsorption. SGLT2 inhibitors (SGLT2i), have shown potential benefits beyond cardiac and renal improvement in preventing and treating cognitive impairment (CI), including mild cognitive impairment, Alzheimer’s disease and vascular dementia in T2DM patients. Studies suggest that SGLT2i may ameliorate diabetic CI through metabolism pathways, inflammation, oxidative stress, neurotrophic factors and AChE inhibition. Clinical trials and meta-analyses have reported significant and insignificant results. Given their vascular effects, SGLT2i may offer unique protection against vascular CI. This review compiles mechanisms and clinical evidence, emphasizing the need for future analysis, evaluation, trials and meta-analyses to verify and recommend optimal SGLT2i selection and dosage for specific patients. Full article
(This article belongs to the Section Endocrinology and Metabolism Research)
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34 pages, 21673 KiB  
Review
Paying Homage to Microvessel Remodeling and Small Vessel Disease in Neurodegeneration: Implications for the Development of Late-Onset Alzheimer’s Disease
by Melvin R. Hayden
J. Vasc. Dis. 2024, 3(4), 419-452; https://doi.org/10.3390/jvd3040033 - 20 Nov 2024
Cited by 1 | Viewed by 2045
Abstract
The microvessel neurovascular unit, with its brain endothelial cells (BEC) and blood–brain barrier remodeling, is important in the development of impaired cognition in sporadic or late-onset Alzheimer’s disease (LOAD), which is associated with aging and is highly prevalent in older populations (≥65 years [...] Read more.
The microvessel neurovascular unit, with its brain endothelial cells (BEC) and blood–brain barrier remodeling, is important in the development of impaired cognition in sporadic or late-onset Alzheimer’s disease (LOAD), which is associated with aging and is highly prevalent in older populations (≥65 years of age). It is also linked with vascular dementia and vascular contributions to cognitive impairment and dementia, including cerebral amyloid angiopathy in neurodegeneration. LOAD is considered to be the number one cause of dementia globally; however, when one considers the role of mixed dementia (MD)—the combination of both the amyloid cascade hypothesis and the vascular hypothesis of LOAD—it becomes apparent that MD is the number one cause. Microvessel BECs are the first cells in the brain to be exposed to peripheral neurotoxins from the systemic circulation and are therefore the brain cells at the highest risk for early and chronic injury. Therefore, these cells are the first to undergo injury, followed by excessive and recurrent wound healing and remodeling processes in aging and other age-related diseases such as cerebrocardiovascular disease, hypertension, type 2 diabetes mellitus, and Parkinson’s disease. This narrative review explores the intricate relationship between microvessel remodeling, cerebral small vessel disease (SVD), and neurodegeneration in LOAD. It also discusses the current understanding of how microvessel dysfunction, disruption, and pathology contribute to the pathogenesis of LOAD and highlights potential avenues for therapeutic intervention. Full article
(This article belongs to the Section Neurovascular Diseases)
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85 pages, 12432 KiB  
Review
Alzheimer’s Disease, Obesity, and Type 2 Diabetes: Focus on Common Neuroglial Dysfunctions (Critical Review and New Data on Human Brain and Models)
by Adolfo Toledano, Arantxa Rodríguez-Casado, María Isabel Älvarez and Adolfo Toledano-Díaz
Brain Sci. 2024, 14(11), 1101; https://doi.org/10.3390/brainsci14111101 - 30 Oct 2024
Cited by 6 | Viewed by 4037
Abstract
Background/Objectives. Obesity, type 2 diabetes (T2D), and Alzheimer’s disease (AD) are pathologies that affect millions of people worldwide. They have no effective therapy and are difficult to prevent and control when they develop. It has been known for many years that these diseases [...] Read more.
Background/Objectives. Obesity, type 2 diabetes (T2D), and Alzheimer’s disease (AD) are pathologies that affect millions of people worldwide. They have no effective therapy and are difficult to prevent and control when they develop. It has been known for many years that these diseases have many pathogenic aspects in common. We highlight in this review that neuroglial cells (astroglia, oligodendroglia, and microglia) play a vital role in the origin, clinical–pathological development, and course of brain neurodegeneration. Moreover, we include the new results of a T2D-AD mouse model (APP+PS1 mice on a high-calorie diet) that we are investigating. Methods. Critical bibliographic revision and biochemical neuropathological study of neuroglia in a T2D-AD model. Results. T2D and AD are not only “connected” by producing complex pathologies in the same individual (obesity, T2D, and AD), but they also have many common pathogenic mechanisms. These include insulin resistance, hyperinsulinemia, hyperglycemia, oxidative stress, mitochondrial dysfunction, and inflammation (both peripheral and central—or neuroinflammation). Cognitive impairment and AD are the maximum exponents of brain neurodegeneration in these pathological processes. both due to the dysfunctions induced by metabolic changes in peripheral tissues and inadequate neurotoxic responses to changes in the brain. In this review, we first analyze the common pathogenic mechanisms of obesity, T2D, and AD (and/or cerebral vascular dementia) that induce transcendental changes and responses in neuroglia. The relationships between T2D and AD discussed mainly focus on neuroglial responses. Next, we present neuroglial changes within their neuropathological context in diverse scenarios: (a) aging involution and neurodegenerative disorders, (b) human obesity and diabetes and obesity/diabetes models, (c) human AD and in AD models, and (d) human AD-T2D and AD-T2D models. An important part of the data presented comes from our own studies on humans and experimental models over the past few years. In the T2D-AD section, we included the results of a T2D-AD mouse model (APP+PS1 mice on a high-calorie diet) that we investigated, which showed that neuroglial dysfunctions (astrocytosis and microgliosis) manifest before the appearance of amyloid neuropathology, and that the amyloid pathology is greater than that presented by mice fed a normal, non-high-caloric diet A broad review is finally included on pharmacological, cellular, genic, and non-pharmacological (especially diet and lifestyle) neuroglial-related treatments, as well as clinical trials in a comparative way between T2D and AD. These neuroglial treatments need to be included in the multimodal/integral treatments of T2D and AD to achieve greater therapeutic efficacy in many millions of patients. Conclusions. Neuroglial alterations (especially in astroglia and microglia, cornerstones of neuroinflammation) are markedly defining brain neurodegeneration in T2D and A, although there are some not significant differences between each of the studied pathologies. Neuroglial therapies are a very important and p. promising tool that are being developed to prevent and/or treat brain dysfunction in T2D-AD. The need for further research in two very different directions is evident: (a) characterization of the phenotypic changes of astrocytes and microglial cells in each region of the brain and in each phase of development of each isolated and associated pathology (single-cell studies are mandatory) to better understand the pathologies and define new therapeutic targets; (b) studying new therapeutic avenues to normalize the function of neuroglial cells (preventing neurotoxic responses and/or reversing them) in these pathologies, as well as the phenotypic characteristics in each moment of the course and place of the neurodegenerative process. Full article
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10 pages, 1517 KiB  
Review
Pathogenesis of Cerebral Small Vessel Disease: Role of the Glymphatic System Dysfunction
by Dong-Hun Lee, Eun Chae Lee, Sang-Won Park, Ji Young Lee, Man Ryul Lee and Jae Sang Oh
Int. J. Mol. Sci. 2024, 25(16), 8752; https://doi.org/10.3390/ijms25168752 - 11 Aug 2024
Cited by 7 | Viewed by 3504
Abstract
Cerebral small vessel disease (CSVD) is a group of pathologies that affect the cerebral blood vessels. CSVD accounts for 25% of strokes and contributes to 45% of dementia. However, the pathogenesis of CSVD remains unclear, involving a variety of complex mechanisms. CSVD may [...] Read more.
Cerebral small vessel disease (CSVD) is a group of pathologies that affect the cerebral blood vessels. CSVD accounts for 25% of strokes and contributes to 45% of dementia. However, the pathogenesis of CSVD remains unclear, involving a variety of complex mechanisms. CSVD may result from dysfunction in the glymphatic system (GS). The GS contains aquaporin-4 (AQP-4), which is in the perivascular space, at the endfeet of the astrocyte. The GS contributes to the removal of waste products from the central nervous system, occupying perivascular spaces and regulating the exchange and movement of cerebrospinal fluid and interstitial fluid. The GS involves astrocytes and aquaporin channels, which are components of the blood–brain barrier, and problems with them may constitute the pathogenesis of CSVD. Vascular risk factors, including diabetes, dilate the perivascular space, disrupting the glymphatic system and the active regulation of AQP-4. CSVD exacerbation due to disorders of the GS is associated with multiple vasculopathies. Dysfunction of the glymphatic system and AQP-4 interferes with the functioning of the blood–brain barrier, which exacerbates CSVD. In a long-term follow-up of CSVD patients with microbleeds, lacunar infarcts, and white matter hyperintensity, several vascular risk factors, including hypertension, increased the risk of ischemic stroke. Dysfunction of the GS may be the cause of CSVD; however, the underlying treatment needs to be studied further. Full article
(This article belongs to the Special Issue Molecular Researches on Ischemic Stroke—2nd Edition)
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13 pages, 920 KiB  
Article
Association between Age at Diagnosis of Type 2 Diabetes and Subsequent Risk of Dementia and Its Major Subtypes
by Da Hea Seo, Mina Kim, Yongin Cho, Seong Hee Ahn, Seongbin Hong and So Hun Kim
J. Clin. Med. 2024, 13(15), 4386; https://doi.org/10.3390/jcm13154386 - 26 Jul 2024
Cited by 2 | Viewed by 1681
Abstract
Background/Objectives: Type 2 diabetes mellitus (T2DM) is a major contributor to cognitive decline and dementia in older adults; however, the role of the age of onset of T2DM in younger patients remains uncertain. We explored the association between the risk of dementia [...] Read more.
Background/Objectives: Type 2 diabetes mellitus (T2DM) is a major contributor to cognitive decline and dementia in older adults; however, the role of the age of onset of T2DM in younger patients remains uncertain. We explored the association between the risk of dementia and its subtypes in relation to the age at T2DM diagnosis. Methods: This population cohort study included a total of 612,201 newly diagnosed T2DM patients. The controls were randomly selected from the general population and matched at a 1:2 ratio based on the propensity score. The outcomes of interest were all-cause dementia, Alzheimer’s disease (AD), and vascular dementia (VD). The association of T2DM with dementia was stratified by the age at diagnosis of T2DM. Results: The mean ages of the subjects in the T2DM and control groups were 55.7 ± 13.0 and 55.7 ± 13.0. The patients with T2DM diagnosed at <50 years had the highest excess risk for most outcomes relative to the controls, with a hazard ratio (HR) (95% CI) of 3.29 (3.11–3.49) for all-cause dementia, 4.08 (3.18–5.24) for AD, and 5.82 (3.84–8.81) for VD. All risks were attenuated progressively with each increasing decade at the diagnostic age, but remained significant; for T2DM diagnosed at ≥80 years, the HR (95% CI) was 1.38 (1.34–1.41) for all-cause dementia, 1.35 (1.31–1.40) for AD, and 1.98 (1.70–2.30) for VD. Conclusions: We need to stratify T2DM management according to the age of diagnosis. Physicians should closely monitor cognitive function in patients with T2DM, especially in younger individuals. Full article
(This article belongs to the Section Endocrinology & Metabolism)
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14 pages, 1210 KiB  
Article
From Mild Cognitive Impairment to Dementia: The Impact of Comorbid Conditions on Disease Conversion
by Federico Menegon, Fabiola De Marchi, Davide Aprile, Iacopo Zanelli, Greta Decaroli, Cristoforo Comi and Giacomo Tondo
Biomedicines 2024, 12(8), 1675; https://doi.org/10.3390/biomedicines12081675 - 26 Jul 2024
Cited by 4 | Viewed by 2553
Abstract
The conversion from mild cognitive impairment (MCI) to dementia is influenced by several factors, including comorbid conditions such as metabolic and vascular diseases. Understanding the impact of these comorbidities can help in the disease management of patients with a higher risk of progressing [...] Read more.
The conversion from mild cognitive impairment (MCI) to dementia is influenced by several factors, including comorbid conditions such as metabolic and vascular diseases. Understanding the impact of these comorbidities can help in the disease management of patients with a higher risk of progressing to dementia, improving outcomes. In the current study, we aimed to analyze data from a large cohort of MCI (n = 188) by principal component analysis (PCA) and cluster analysis (CA) to classify patients into distinct groups based on their comorbidity profile and to predict the risk of conversion to dementia. From our analysis, four clusters emerged. CA showed a significantly higher rate of disease progression for Cluster 1, which was predominantly characterized by extremely high obesity and diabetes compared to other clusters. In contrast, Cluster 3, which was defined by a lower prevalence of all comorbidities, had a lower conversion rate. Cluster 2, mainly including subjects with traumatic brain injuries, showed the lowest rate of conversion. Lastly, Cluster 4, including a high load of hearing loss and depression, showed an intermediate risk of conversion. This study underscores the significant impact of specific comorbidity profiles on the progression from MCI to dementia, highlighting the need for targeted interventions and management strategies for individuals with these comorbidity profiles to potentially delay or prevent the onset of dementia. Full article
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18 pages, 510 KiB  
Review
Formulating Treatment to Cure Alzheimer’s Dementia: Approach #2
by Jeffrey Fessel
Int. J. Mol. Sci. 2024, 25(6), 3524; https://doi.org/10.3390/ijms25063524 - 20 Mar 2024
Cited by 2 | Viewed by 2462
Abstract
There are two generic approaches to curing any medical condition. The first one treats every patient for all the known possible causes that contribute to pathogenesis; the second one individualizes potentially curative therapy by only identifying in each separate patient the components of [...] Read more.
There are two generic approaches to curing any medical condition. The first one treats every patient for all the known possible causes that contribute to pathogenesis; the second one individualizes potentially curative therapy by only identifying in each separate patient the components of pathogenesis that are actually operative and treating those. This article adopts the second approach for formulating a cure for Alzheimer’s dementia (AD). The components of AD’s pathogenesis are, in alphabetical order, as follows: circadian rhythm disturbances, depression, diabetes and insulin resistance, dyslipidemia, hypertension, inflammation, metabolic syndrome, mitochondrial dysfunction, nutritional deficiencies, TGF-β deficiency, underweight, vascular abnormalities, and Wnt/β-catenin deficiency. For each component, data are described that show the degree to which its prevalence is higher in patients with mild cognitive impairment (MCI) who did not revert to having normal cognition than in those who did because the former group is the pool of patients in which future AD may develop. Only addressing the components that are present in a particular individual potentially is a curative strategy. Published data indicate that curative therapy requires the number of such components that are addressed to be ≥3. Although structural brain changes cannot be directly addressed, the impaired neural tracts result from many of the reversible causal elements, so correcting them will benefit these tracts. Full article
17 pages, 1513 KiB  
Review
Cognitive Impairment and Brain Atrophy in Patients with Chronic Kidney Disease
by Kazuhiko Tsuruya and Hisako Yoshida
J. Clin. Med. 2024, 13(5), 1401; https://doi.org/10.3390/jcm13051401 - 28 Feb 2024
Cited by 8 | Viewed by 2965
Abstract
In Japan, the aging of the population is rapidly accelerating, with an increase in patients with chronic kidney disease (CKD) and those undergoing dialysis. As a result, the number of individuals with cognitive impairment (CI) is rising, and addressing this issue has become [...] Read more.
In Japan, the aging of the population is rapidly accelerating, with an increase in patients with chronic kidney disease (CKD) and those undergoing dialysis. As a result, the number of individuals with cognitive impairment (CI) is rising, and addressing this issue has become an urgent problem. A notable feature of dementia in CKD patients is the high frequency of vascular dementia, making its prevention through the management of classical risk factors such as hypertension, diabetes mellitus, dyslipidemia, smoking, etc., associated with atherosclerosis and arteriosclerosis. Other effective measures, including the use of renin–angiotensin system inhibitors, addressing anemia, exercise therapy, and lifestyle improvements, have been reported. The incidence and progression of CI may also be influenced by the type of kidney replacement therapy, with reports suggesting that long-duration dialysis, low-temperature hemodialysis, peritoneal dialysis, and kidney transplantation can have a preferable effect on the preservation of cognitive function. In conclusion, patients with CKD are at a higher risk of developing CI, with brain atrophy being a contributing factor. Despite the identification of various preventive measures, the evidence substantiating their efficacy remains limited across all studies. Future expectations lie in large-scale randomized controlled trials. Full article
(This article belongs to the Section Brain Injury)
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28 pages, 783 KiB  
Article
Immunological Profile and Markers of Endothelial Dysfunction in Elderly Patients with Cognitive Impairments
by Nikolay V. Goncharov, Polina I. Popova, Igor V. Kudryavtsev, Alexey S. Golovkin, Irina V. Savitskaya, Piotr P. Avdonin, Ekaterina A. Korf, Natalia G. Voitenko, Daria A. Belinskaia, Maria K. Serebryakova, Natalia V. Matveeva, Natalia O. Gerlakh, Natalia E. Anikievich, Marina A. Gubatenko, Irina A. Dobrylko, Andrey S. Trulioff, Arthur D. Aquino, Richard O. Jenkins and Pavel V. Avdonin
Int. J. Mol. Sci. 2024, 25(3), 1888; https://doi.org/10.3390/ijms25031888 - 4 Feb 2024
Cited by 11 | Viewed by 3388
Abstract
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 [...] Read more.
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. Full article
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25 pages, 1173 KiB  
Review
Inflammatory Pathways in Overweight and Obese Persons as a Potential Mechanism for Cognitive Impairment and Earlier Onset Alzeihmer’s Dementia in the General Population: A Narrative Review
by Alexandru Dan Costache, Bogdan Emilian Ignat, Cristina Grosu, Alexandra Mastaleru, Irina Abdulan, Andra Oancea, Mihai Roca, Maria Magdalena Leon, Minerva Codruta Badescu, Stefana Luca, Alexandru Raul Jigoranu, Adriana Chetran, Ovidiu Mitu, Irina Iuliana Costache and Florin Mitu
Biomedicines 2023, 11(12), 3233; https://doi.org/10.3390/biomedicines11123233 - 6 Dec 2023
Cited by 7 | Viewed by 3403
Abstract
The overweight status or obesity can be confirmed through classical methods such as the body mass index (BMI) and the waist-to-hip ratio (WHR). Apart from metabolic issues such as atherosclerosis, liver steatosis, or diabetes mellitus, long-term obesity or overweight status can pose a [...] Read more.
The overweight status or obesity can be confirmed through classical methods such as the body mass index (BMI) and the waist-to-hip ratio (WHR). Apart from metabolic issues such as atherosclerosis, liver steatosis, or diabetes mellitus, long-term obesity or overweight status can pose a risk for cardiovascular and neurovascular complications. While some acute adverse events like coronary syndromes of strokes are well-documented to be linked to an increased body mass, there are also chronic processes that, due to their silent onset and evolution, are underdiagnosed and not as thoroughly studied. Through this review, we aimed to collect all relevant data with regard to the long-term impact of obesity on cognitive function in all ages and its correlation with an earlier onset of dementia such as Alzheimer’s disease (AD). The exact mechanisms through which a decline in cognitive functions occurs in overweight or obese persons are still being discussed. A combination of factors has been acknowledged as potential triggers, such as a sedentary lifestyle and stress, as well as a genetic predisposition, for example, the apolipoprotein E (ApoE) alleles in AD. Most research highlights the impact of vascular dysfunction and systemic inflammation on the nervous system in patients with obesity and the subsequent neurological changes. Obesity during the early to mid-ages leads to an earlier onset of cognitive dysfunction in various forms. Also, lifestyle intervention can reverse cognitive dysfunction, especially dieting, to encourage weight loss. Full article
(This article belongs to the Section Endocrinology and Metabolism Research)
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19 pages, 812 KiB  
Review
Unravelling the Threads: A Brief Insight into Vascular Dementia
by Syed Haris Omar
J. Vasc. Dis. 2023, 2(4), 419-437; https://doi.org/10.3390/jvd2040033 - 2 Nov 2023
Cited by 2 | Viewed by 3720
Abstract
Vascular dementia (VaD), characterized by cognitive decline attributable to cerebrovascular disease, is the second most common type of dementia after Alzheimer’s disease. This review aims to explore the prevalent risk factors, pharmacological interventions, and non-pharmacotherapeutic strategies associated with the condition. Recognized risk factors [...] Read more.
Vascular dementia (VaD), characterized by cognitive decline attributable to cerebrovascular disease, is the second most common type of dementia after Alzheimer’s disease. This review aims to explore the prevalent risk factors, pharmacological interventions, and non-pharmacotherapeutic strategies associated with the condition. Recognized risk factors include advanced age, hypertension, diabetes mellitus, obesity, and hyperlipidemia with emerging evidence implicating additional lifestyle and genetic factors. Pharmacotherapy for VaD mainly focuses on managing these underlying risk factors, coupled with symptomatic treatments. Therapeutic agents commonly used include antihypertensives, statins, antiplatelet drugs, antidiabetic agents, and specific cognitive enhancers like cholinesterase inhibitors. However, the effectiveness of these treatments remains under continuous study, underscoring the need for comprehensive, individualized treatment plans. Non-pharmacotherapeutic strategies, encompassing lifestyle modifications such as diet and exercise have gained considerable attention. They have shown promise in improving cognitive function and enhancing the quality of life in patients with VaD. The application of a multi-domain intervention approach may provide a more holistic management strategy for VaD. Further research is needed to define the best practices in both pharmacotherapy and non-pharmacotherapy treatments, considering the multifactorial and heterogeneous nature of this condition. Full article
(This article belongs to the Section Neurovascular Diseases)
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20 pages, 1794 KiB  
Review
Physiological Mechanisms Inherent to Diabetes Involved in the Development of Dementia: Alzheimer’s Disease
by Himan Mohamed-Mohamed, Victoria García-Morales, Encarnación María Sánchez Lara, Anabel González-Acedo, Teresa Pardo-Moreno, María Isabel Tovar-Gálvez, Lucía Melguizo-Rodríguez and Juan José Ramos-Rodríguez
Neurol. Int. 2023, 15(4), 1253-1272; https://doi.org/10.3390/neurolint15040079 - 10 Oct 2023
Cited by 5 | Viewed by 2853
Abstract
Type 2 diabetes mellitus (T2D) is a metabolic disease reaching pandemic levels worldwide. In parallel, Alzheimer’s disease (AD) and vascular dementia (VaD) are the two leading causes of dementia in an increasingly long-living Western society. Numerous epidemiological studies support the role of T2D [...] Read more.
Type 2 diabetes mellitus (T2D) is a metabolic disease reaching pandemic levels worldwide. In parallel, Alzheimer’s disease (AD) and vascular dementia (VaD) are the two leading causes of dementia in an increasingly long-living Western society. Numerous epidemiological studies support the role of T2D as a risk factor for the development of dementia. However, few basic science studies have focused on the possible mechanisms involved in this relationship. On the other hand, this review of the literature also aims to explore the relationship between T2D, AD and VaD. The data found show that there are several alterations in the central nervous system that may be promoting the development of T2D. In addition, there are some mechanisms by which T2D may contribute to the development of neurodegenerative diseases such as AD or VaD. Full article
(This article belongs to the Topic Translational Advances in Neurodegenerative Dementias)
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12 pages, 2073 KiB  
Article
Astaxanthin: A Marine Drug That Ameliorates Cerebrovascular-Damage-Associated Alzheimer’s Disease in a Zebrafish Model via the Inhibition of Matrix Metalloprotease-13
by Nallupillai Paramakrishnan, Khian Giap Lim, Yamunna Paramaswaran, Nemat Ali, Mohammad Waseem, Gamal A. Shazly, Yousef A. Bin Jardan and Arunachalam Muthuraman
Mar. Drugs 2023, 21(8), 433; https://doi.org/10.3390/md21080433 - 31 Jul 2023
Cited by 7 | Viewed by 3256
Abstract
Alzheimer’s disease (AD) is a major type of dementia disorder. Common cognitive changes occur as a result of cerebrovascular damage (CVD) via the disruption of matrix metalloproteinase-13 (MMP-13). In diabetic cases, the progress of vascular dementia is faster and the AD rate is [...] Read more.
Alzheimer’s disease (AD) is a major type of dementia disorder. Common cognitive changes occur as a result of cerebrovascular damage (CVD) via the disruption of matrix metalloproteinase-13 (MMP-13). In diabetic cases, the progress of vascular dementia is faster and the AD rate is higher. Patients with type 2 diabetes are known to have a higher risk of the factor for AD progression. Hence, this study is designed to investigate the role of astaxanthin (AST) in CVD-associated AD in zebrafish via the inhibition of MMP-13 activity. CVD was developed through the intraperitoneal and intracerebral injection of streptozotocin (STZ). The AST (10 and 20 mg/L), donepezil (1 mg/L), and MMP-13 inhibitor (i.e., CL-82198; 10 μM) were exposed for 21 consecutive days in CVD animals. The cognitive changes in zebrafish were evaluated through light and dark chamber tests, a color recognition test, and a T-maze test. The biomarkers of AD pathology were assessed via the estimation of the cerebral extravasation of Evans blue, tissue nitrite, amyloid beta-peptide aggregation, MMP-13 activity, and acetylcholinesterase activity. The results revealed that exposure to AST leads to ameliorative behavioral and biochemical changes. Hence, AST can be used for the management of AD due to its multi-targeted actions, including MMP-13 inhibition. Full article
(This article belongs to the Special Issue Marine Compounds as Anti-Alzheimer's Agent)
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