Abstract:ObjectiveThis study investigated the effects of intervention with a combination of nutrients in the amyloid precursor protein-presenilin (APP-PSN) C57BL/6J double transgenic mouse model of Alzheimer’s disease (AD).MethodsA total of 72 2-month-old APP-PSN mice were randomly assigned to three groups. The model group (MG) was fed regular, unsupplemented chow, while the low- and high-dose treatment groups (LG and HG, respectively) were given a combination of nutrients that included phosphatidylserine, blueberry ex… Show more
“…The former are markers of neuronal and glial function whereas the latter are markers of pathological changes. As stated previously, biomarkers Blueberry supplementation has been shown in some prior studies to benefit cognitive aging and preclinical studies have reported that blueberry bioactives may provide anti-oxidant benefits, enhance microglial clearance of Aβ, inhibit aggregation of Aβ42, or suppress microglial activation and provide protection against Aβ-induced neurotoxicity (reviewed in [7][8][9][10][11][12][13][14][15][16][17]. Blueberry supplementation has also been reported to improve cognition in pilot studies of MCI (16,17).…”
Section: Discussionmentioning
confidence: 89%
“…Practical, well-tolerated, and non-invasive lifestyle interventions are highly desirable for AD prevention in at-risk middle-aged and older adults (3)(4)(5)(6)(7)(8)(9). Evidence from epidemiological, pre-clinical and pilot clinical studies suggests that regular consumption of blueberries may protect against cognitive decline or dementia (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Blueberries contain high levels of micronutrients and antioxidants (such as anthrocyanins) which in preclinical studies have been found to impact many pathways involved in cognitive function or dementia risk -such as reduced oxidative stress, improved inflammatory response, reversed age-related decrements in cognition, increased cerebral blood flow, enhanced microglial clearance of Aβ, inhibited aggregation of Aβ42, suppressed microglial activation and protection against Aβ-induced neurotoxicity (reviewed in 7,[12][13][14][15][16][17].…”
mentioning
confidence: 99%
“…Evidence from epidemiological, pre-clinical and pilot clinical studies suggests that regular consumption of blueberries may protect against cognitive decline or dementia (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Blueberries contain high levels of micronutrients and antioxidants (such as anthrocyanins) which in preclinical studies have been found to impact many pathways involved in cognitive function or dementia risk -such as reduced oxidative stress, improved inflammatory response, reversed age-related decrements in cognition, increased cerebral blood flow, enhanced microglial clearance of Aβ, inhibited aggregation of Aβ42, suppressed microglial activation and protection against Aβ-induced neurotoxicity (reviewed in 7,[12][13][14][15][16][17]. Some, but not all, epidemiological studies have found evidence favoring a protective role of blueberry consumption on cognition or AD risk.…”
Background
There is a need to develop non-invasive practical lifestyle interventions for preventing Alzheimer’s disease (AD) in people at risk, such as those with mild cognitive impairment (MCI). Blueberry consumption has been associated with reduced risk of dementia in some epidemiologic studies and with improvements in cognition in healthy aging adults. Blood-based biomarkers have emerged at the forefront of AD therapeutics research spurred by the development of reliable ultra-sensitive “single-molecule array” assays with 100-1000-fold greater sensitivity over traditional platforms.
Objective
The purpose of this study was to examine the effect of blueberry supplementation in MCI on six blood biomarkers: amyloid-beta 40 (Aβ40), amyloid-beta 42 (Aβ42), phosphorylated Tau181 (ptau181), neurofilament light (NfL), Glial Fibrillary acidic protein (GFAP), and Brain-Derived Neurotrophic Factor (BDNF).
Methods
This was a 12-week, open-label, pilot trial of 10 participants with MCI (mean age 80.2 years + 5.16). Subjects consumed 36 grams per day of lyophilized blueberry powder in a split dose consumed with breakfast and dinner. Baseline and endpoint venous blood was analyzed using an ultrasensitive SIMOA assay. Our aim was to test if blueberry supplementation would particularly impact p-tau181, NfL, and GFAP elevations associated with the neurodegenerative process.
Results
There were no statistically significant (p < 0.05) changes from baseline to endpoint for any of the biomarker values or in the ratios of Aβ42 / Aβ40 and ptau181/ Aβ42. Adverse effects were mild and transient; supplementation was relatively well tolerated with all subjects completing the study.
Conclusion
To our knowledge, this is the first study to prospectively examine the effects of blueberry supplementation on a panel of blood biomarkers reflecting the neurodegenerative process. Our findings raise two possibilities - a potential stabilization of the neurodegenerative process or a lack of a direct and acute effect on beta-amyloid/tau/glial markers. A larger controlled study is warranted.
“…The former are markers of neuronal and glial function whereas the latter are markers of pathological changes. As stated previously, biomarkers Blueberry supplementation has been shown in some prior studies to benefit cognitive aging and preclinical studies have reported that blueberry bioactives may provide anti-oxidant benefits, enhance microglial clearance of Aβ, inhibit aggregation of Aβ42, or suppress microglial activation and provide protection against Aβ-induced neurotoxicity (reviewed in [7][8][9][10][11][12][13][14][15][16][17]. Blueberry supplementation has also been reported to improve cognition in pilot studies of MCI (16,17).…”
Section: Discussionmentioning
confidence: 89%
“…Practical, well-tolerated, and non-invasive lifestyle interventions are highly desirable for AD prevention in at-risk middle-aged and older adults (3)(4)(5)(6)(7)(8)(9). Evidence from epidemiological, pre-clinical and pilot clinical studies suggests that regular consumption of blueberries may protect against cognitive decline or dementia (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Blueberries contain high levels of micronutrients and antioxidants (such as anthrocyanins) which in preclinical studies have been found to impact many pathways involved in cognitive function or dementia risk -such as reduced oxidative stress, improved inflammatory response, reversed age-related decrements in cognition, increased cerebral blood flow, enhanced microglial clearance of Aβ, inhibited aggregation of Aβ42, suppressed microglial activation and protection against Aβ-induced neurotoxicity (reviewed in 7,[12][13][14][15][16][17].…”
mentioning
confidence: 99%
“…Evidence from epidemiological, pre-clinical and pilot clinical studies suggests that regular consumption of blueberries may protect against cognitive decline or dementia (7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Blueberries contain high levels of micronutrients and antioxidants (such as anthrocyanins) which in preclinical studies have been found to impact many pathways involved in cognitive function or dementia risk -such as reduced oxidative stress, improved inflammatory response, reversed age-related decrements in cognition, increased cerebral blood flow, enhanced microglial clearance of Aβ, inhibited aggregation of Aβ42, suppressed microglial activation and protection against Aβ-induced neurotoxicity (reviewed in 7,[12][13][14][15][16][17]. Some, but not all, epidemiological studies have found evidence favoring a protective role of blueberry consumption on cognition or AD risk.…”
Background
There is a need to develop non-invasive practical lifestyle interventions for preventing Alzheimer’s disease (AD) in people at risk, such as those with mild cognitive impairment (MCI). Blueberry consumption has been associated with reduced risk of dementia in some epidemiologic studies and with improvements in cognition in healthy aging adults. Blood-based biomarkers have emerged at the forefront of AD therapeutics research spurred by the development of reliable ultra-sensitive “single-molecule array” assays with 100-1000-fold greater sensitivity over traditional platforms.
Objective
The purpose of this study was to examine the effect of blueberry supplementation in MCI on six blood biomarkers: amyloid-beta 40 (Aβ40), amyloid-beta 42 (Aβ42), phosphorylated Tau181 (ptau181), neurofilament light (NfL), Glial Fibrillary acidic protein (GFAP), and Brain-Derived Neurotrophic Factor (BDNF).
Methods
This was a 12-week, open-label, pilot trial of 10 participants with MCI (mean age 80.2 years + 5.16). Subjects consumed 36 grams per day of lyophilized blueberry powder in a split dose consumed with breakfast and dinner. Baseline and endpoint venous blood was analyzed using an ultrasensitive SIMOA assay. Our aim was to test if blueberry supplementation would particularly impact p-tau181, NfL, and GFAP elevations associated with the neurodegenerative process.
Results
There were no statistically significant (p < 0.05) changes from baseline to endpoint for any of the biomarker values or in the ratios of Aβ42 / Aβ40 and ptau181/ Aβ42. Adverse effects were mild and transient; supplementation was relatively well tolerated with all subjects completing the study.
Conclusion
To our knowledge, this is the first study to prospectively examine the effects of blueberry supplementation on a panel of blood biomarkers reflecting the neurodegenerative process. Our findings raise two possibilities - a potential stabilization of the neurodegenerative process or a lack of a direct and acute effect on beta-amyloid/tau/glial markers. A larger controlled study is warranted.
“…Meanwhile, a combination of nutrients like phosphatidylserine, blueberry extracts, docosahexaenoic acid (DHA), and eicosapentaenoic acid (EPA) are categorized under omega-3 fatty acids was also found to increase the level of acetylcholine by reducing the total cholinesterase (TChE) level in the brain of the AD transgenic mouse model [51]. Altogether, this supplementation improves memory and cognitive function and can be recommended as a complementary therapy for cognitive decline.…”
Section: Nutraceuticals Effects On the Inhibition Of Reuptake Enzymesmentioning
“…Generally, it is acknowledged that MI is closely related to oxygen radicals, vascular endothelial injury, and myocardial cell apoptosis [ 4 ]. Moreover, cardiomyocyte apoptosis and necrosis triggered by MI result in the loss of cardiomyocytes, which may further lead to a significant decrease in heart pumping and congestive heart failure [ 5 ]. Previous research has shown that timely reperfusion treatment for acute myocardial infarction (AMI), by shrinking the myocardial necrosis zone, may cause reperfusion injury [ 6 – 11 ].…”
BackgroundThis study was designed to investigate the effects of microRNA-92 (miR-92), Kruppel-like factor 2 (KLF2), and Kruppel-like factor 4 (KLF4) on endothelial injury after acute myocardial infarction (AMI).Material/MethodsBlood samples were collected from 50 AMI patients for detection of cardiac troponin I (cTnI), heart-type fatty acid-binding protein (H-FABP), and von Willebrand factor (vWF). The Sprague-Dawley rat models of AMI (n=30) were established by ligating their left anterior descending coronary artery. The cardiac markers of AMI patients and rat models were analyzed with enzyme-linked immunosorbent assay and immunohistochemistry. Human umbilical vein endothelial cells were processed into 5 groups: control, negative control, miR-92a inhibitors, miR-92a inhibitors + KLF2 small interfering RNA (siRNA), and miR-92a inhibitors + KLF4 siRNA. Cell proliferation and apoptosis were detected using MTT assay and flow cytometry. RT-PCR and Western blot were conducted to analyze KLF2 and KLF4 expressions.ResultsAMI patients exhibited significantly higher expression of both endothelial injury markers (e.g., cTnI, H-FABP, vWF) and miR-92a in blood samples, when compared with controls (P<0.05). Model rats also had similar expressional tendencies, along with lower KLF2 and KLF4 expressions (P<0.05). Further, it could be observed in cellular experiments that treatment of miR-92a mimics can further upregulate endothelial injury markers, and miR-92a and both KLF2 and KLF4 were downregulated by miR-92a mimics (all, P<0.05). Also, the luciferase activity assay confirmed the direct binding of miR-92a to 3′ UTR of KLF2/4.ConclusionsMiR-92a was involved in the endothelial injury process after AMI and was able to suppress KLF2 and KLF4 expression.
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