“…9,10 Furthermore, blood components and derivatives have been investigated for potential diagnosis of Alzheimer's disease using spectroscopic techniques. [11][12][13][14] The former mentioned methods are, at least, partially invasive, time consuming and expensive. Nevertheless, even though these assessments are done in vivo and would aid the early diagnosis of AD, a conclusive assessment can only be done post-mortem.…”
Raman spectroscopy was used to examine unstained, formalin fixed Alzheimer's disease human brain tissue to potentially identify a unique spectral signature of amyloid-beta plaques.
“…9,10 Furthermore, blood components and derivatives have been investigated for potential diagnosis of Alzheimer's disease using spectroscopic techniques. [11][12][13][14] The former mentioned methods are, at least, partially invasive, time consuming and expensive. Nevertheless, even though these assessments are done in vivo and would aid the early diagnosis of AD, a conclusive assessment can only be done post-mortem.…”
Raman spectroscopy was used to examine unstained, formalin fixed Alzheimer's disease human brain tissue to potentially identify a unique spectral signature of amyloid-beta plaques.
“…Chronic inflammation, oxidative stress, and changes in cellular energy metabolism participate in reduced kidney function [11][12][13]. Mitochondrial dysfunction and reduced CoQ 10 concentration contribute to dysfunctional platelet activity in diseases, such as neurological diseases, cardiovascular diseases, diabetes mellitus, sepsis, Alzheimer's disease, Parkinson's disease, and chronic kidney disease [5,[14][15][16][17]. CoQ 10 plays a key role in mitochondrial energy production, and it transfers electrons from Complex I and Complex II to Complex III along the respiratory chain in the inner mitochondrial membrane.…”
Section: Discussionmentioning
confidence: 99%
“…As an antioxidant, CoQ 10 quenches free radicals and directly prevents lipid peroxidation [9]. Different studies have demonstrated that platelet mitochondrial dysfunction has also been used for studying mitochondria-related diseases [10][11][12][13][14][15][16][17][18].…”
Chronic kidney disease (CKD) is characterized by a progressive loss of renal function and a decrease of glomerular filtration rate. Reduced mitochondrial function, coenzyme Q10 (CoQ10), and increased oxidative stress in patients with CKD contribute to the disease progression. We tested whether CoQ10 levels, oxidative stress and platelet mitochondrial bioenergetic function differ between groups of CKD patients. Methods: Twenty-seven CKD patients were enrolled in this trial, 17 patients had arterial hypertension (AH) and 10 patients had arterial hypertension and diabetes mellitus (AH and DM). The control group consisted of 12 volunteers. A high-resolution respirometry (HRR) method was used for the analysis of mitochondrial bioenergetics in platelets, and an HPLC method with UV detection was used for CoQ10 determination in platelets, blood, and plasma. Oxidative stress was determined as thiobarbituric acid reactive substances (TBARS). Results: Platelets mitochondrial respiration showed slight, not significant differences between the groups of CKD patients and control subjects. The oxygen consumption by intact platelets positively correlated with the concentration of CoQ10 in the platelets of CKD patients. Conclusion: A decreased concentration of CoQ10 and oxidative stress could contribute to the progression of renal dysfunction in CKD patients. The parameters of platelet respiration assessed by high-resolution respirometry can be used only as a weak biological marker for mitochondrial diagnosis and therapy monitoring in CKD patients.
“…These mechanisms include reducing oxidative stress [105] with concomitant strengthening of anti-oxidant system [106] and anti-inflammatory response or enhanced activity of acetylcholinesterase [107]. AD is associated with decreased mitochondrial biogenesis, which is a characteristic shared by many neurological and psychiatric disorders [108]. In streptozotocin-treated rodents (a well-established murine model of type 2 diabetes, T2D), carnosine treatment improved glucose metabolism as well as spatial recognition memory, retention, and recall, and prevented reduction of step-through latency in a dose-dependent manner [109].…”
Section: Animal Studies Of the Role Of Carnosine In Brain-related mentioning
Neurological, neurodegenerative, and psychiatric disorders represent a serious burden because of their increasing prevalence, risk of disability, and the lack of effective causal/disease-modifying treatments. There is a growing body of evidence indicating potentially favourable effects of carnosine, which is an over-the-counter food supplement, in peripheral tissues. Although most studies to date have focused on the role of carnosine in metabolic and cardiovascular disorders, the physiological presence of this di-peptide and its analogues in the brain together with their ability to cross the blood-brain barrier as well as evidence from in vitro, animal, and human studies suggest carnosine as a promising therapeutic target in brain disorders. In this review, we aim to provide a comprehensive overview of the role of carnosine in neurological, neurodevelopmental, neurodegenerative, and psychiatric disorders, summarizing current evidence from cell, animal, and human cross-sectional, longitudinal studies, and randomized controlled trials.
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