CLA and cognitive function -
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We thank all the participants, health professionals, and researchers, as well as their colleagues in the NILS-LSA, for completing the survey for this study. We also thank those who were involved in the data collection and analyses. This work was supported by the Research Funding for Longevity Sciences from the National Center for Geriatrics and Gerontology, Japan.
I would like to thank Yoshinori Kitagawa Suntory Wellness Ltd. for scientific advice and encouragement. This cohort study based on the NILS-LSA was supported by the National Center for Geriatrics and Gerontology The present study was completed by Suntory Wellness Ltd.
CH, TT, TR, and H Shibata are employees of Suntory Wellness, Ltd. Department of Epidemiology of Aging, National Center for Geriatrics and Gerontology, Morioka-cho, , Obu-City, Aichi, Japan.
Institute for Health Care Science, Suntory Wellness Limited, Seikadai, Seika-cho, Soraku- gun, , Kyoto, Japan. Faculty of Health and Medical Sciences, Aichi Shukutoku University, Katahira, , Nagakute- city, Aichi, Japan. Graduate School of Nutritional Sciences, Nagoya University of Arts and Sciences, 57 Takenoyama, Iwasaki-cho, , Nisshin-city, Aichi, Japan.
You can also search for this author in PubMed Google Scholar. The research was designed by CH, RO, FA, and H Shimokata; the study was implemented by HS Hiroshi Shimokata , FA, and RO; the essential reagents or essential materials were provisioned by H Shimokata, FA, RO, YN, CT, and YK; the data and statistical analyses were carried out by CH; the manuscript was written by CH, RO, YN, CT, YK, TT, TR, H Shibata, FA, and H Shimokata; and RO was responsible for the final content.
All authors read and approved the final manuscript. Correspondence to Rei Otsuka. The Committee of Ethics of Human Research of the National Center for Geriatrics and Gerontology approved this study Approval number: All methods were carried out in accordance with relevant guidelines and regulations and informed consent was obtained from all participants.
This work was supported by Suntory Wellness Ltd. CH, TT, TR, and H Shibata are employees of Suntory Wellness Ltd. Others declare no conflict of interest regarding this study.
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Open Access This article is licensed under a Creative Commons Attribution 4.
The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. Figure 5a presents the results of such an experiment. At 3 months of age, when there is still no measurable cognitive loss in the 5XFAD mice, the COX IV-1 staining was similar to the one observed in normal brains, but two months later 5 months old mice the levels of COX IV-1 in 5XFAD brains were significantly reduced and subsequently there were mostly absent when these mice reached 10 months of age.
Contrarily, brain slices of Nano-PSO treated 10 months old 5XFAD mice presented levels of COX IV-1 similar to the ones observed in WT mice.
Interestingly, 10 months old treated WT mice present a slight elevation of COXIV-1 expression, concomitant with the improved cognitive performance of such mice in the T-maze test. These results resemble the ones obtained for TgMHu2MEK mice modeling for genetic CJD Nano-PSO treatment restored mitochondrial COX IV-1 expression in brains of 5XFAD mice.
a Paraffin embedded brain sections of untreated 5XFAD mice at 3, 5 and 10 months of age , treated Tg 10 months as well as untreated and treated WT 10 months mice were stained with α COX IV-1 mAb red and counterstained with dapi blue. The magnification of cortex area presented in this figure is x b Ten months old 5XFAD mice, treated I and untreated II with Nano-PSO, were double-stained with the 6E10 antibody green and α COX IV-1 mAb red and presented at a magnification of x Magnification of single cells x presented for treated III and untreated IV 5XFAD brains.
Cortical neurons from 10 mounts WT brain also stained with 6E10 and COX IV-1, presented in picture V x The 5XFAD mice used in the current study were reported to display age dependent intraneuronal and mitochondrial Aβ aggregates, as well as extracellular plaques comprising Aβ To investigate the intracellular levels and mitochondrial localization of Aβ in Nano-PSO treated and untreated 5XFAD brains, we co-immunostained 10 months old paraffin embedded brain sections from treated and untreated 5XFAD mice both with the αAβ 6E10 mAb green and with α COX IV-1 red , which is an established mitochondrial enzyme.
Figure 5b shows an intense staining for Aβ green in most cells of the untreated samples. As for the COX IV-1 staining, while in some cells there was no signal whatsoever as seen in Fig.
Contrarily, in the panel for the Nano-PSO treated brain samples, Aβ levels were significantly lower, and the stronger COX IV-1 signal was mostly red, indicating Aβ levels in mitochondria have been reduced by the treatment. This is an interesting result indicating a significant difference between the effect of Nano-PSO on 5XFAD mice as compared to TgMHu2MEK mice While in both models of neurodegeneration COX IV-1 expression was restored by Nano-PSO administration, only in the AD model Nano-PSO reduced the levels of the aberrant protein aggregates.
To evaluate whether treatment with Nano-PSO could reduce the amyloid plaque burden in 5XFAD mice we immunostained Aβ plaques in brains of untreated Tg mice of different ages as well as in 10 months old Nano-PSO treated 5XFAD mice both by immunohistochemistry and by thioflavin S In untreated 5XFAD mice, the levels of Aβ plaques in brains increased in an age-dependent manner 37 see Fig.
As can be seen in Fig. Similar results were obtained by thioflavin S staining Fig. Amyloid plaque burden is decreased in brains of Nano-PSO treated 5XFAD mice. e Sagittal section of 10 months 5Xfad mice, treated and untreated, were stain with Thioflavin S, to label dense-core plaques in cortex x Next, we evaluated the levels of APP and Aβ by immunoblotting.
APP is a single transmembrane glycoprotein located in most brain regions. Cleavage of APP by beta and gamma secretase yield the A-beta peptide, a toxic fragment which contains 40 or 42 amino acids that can aggregates to form flexible soluble oligomers which may exist in several forms Brain samples from WT and 5XFAD Nano-PSO treated or untreated mice at several ages were subjected to SDS page by a protocol described in the methods, and subsequently immunoblotted with the αAβ 6E10 antibody, which recognizes human APP as expressed in the 5XFAD transgene, but not mouse APP as expressed in WT mice.
Figure 7 presents the results of these experiments. Most important, and concomitant with the reduced number of plaques as seen in Fig. We therefore conclude that long-term administration of Nano-PSO resulted in a significant decrease in both intracellular and extracellular Aβ levels. Decreased levels of Aβ in brains of 5XFAD mice treated with Nano-PSO.
Brain homogenates of WT, untreated and treated 5XFAD transgenic mice were immunoblotted with the anti Aβ 6E10mAb. Figure a shows levels of APP and Aβ oligomers. Figure b shows Aβ monomers in brains. Beta-actin served as loading control lower panel of b. In some cases, blots have been cropped and increased in exposure; full length original blots are presented in Supplementary Fig.
Figure c represent quantitative analysis of immunoreactive bands. The bars represent the relative levels of Aβ compared with beta actin and are expressed as percentage of the 3m WT value. We have shown above that following Nano-PSO administration, CLA, an conjugated fatty acid recognized as a calpain inhibitor 20 , accumulates in the brains of Nano-PSO treated mice.
This is a unique effect which does not occur following administration of PSO or CLA in their native forms to animals 17 , 18 , Inhibition of calpain activity is acknowledged today as a potential target in the search of treatments for neurodegenerative diseases since high activity of calpain and the subsequent accumulation of its product, p25, is a feature in diseases such as AD and PD 8 , Brain accumulation of p25 was also shown in the 5XFAD model We also immunoblotted with the same antibody brain sampled from Nano-PSO treated and untreated TGMHu2MEK mice 13 , 15 , to establish whether p25 can also serve as a marker for neurodegeneration and treatment success in genetic prion diseases.
Figure 8 shows that the levels of p25 are low in young WT mice and 5XFAD mice, then increase significantly in the clinical stages of both 5XFAD and TgMHu2MEK mice.
In both animal models, mimicking AD and gCJD respectively 13 , 21 , p25 was reduced following long-term Nano-PSO treatment, concomitantly with clinical improvement and reduction of oxidative stress damage. Nano-PSO treatment reduced p25 levels in neurodegenerative brains.
Blots have been cropped for conciseness; full length original blots are presented in Supplementary Fig. b Quantitative analysis of immunoreactive bands of p We have shown in this work that administration of Nano-PSO, a Nano-formulation of PSO previously shown to delay disease progression in a genetic model of CJD as well as in EAE 40 , resulted in incorporation of substantial levels of CLA into the brains of treated mice.
These results are in contrast with those obtained for animals treated with PSO, following which, as previously described 17 , 19 , no PA and only traces of CLA were detected in brains of treated animals.
CLA, a metabolite of PA, was also absent from the brains of mice treated with other oils comprising Punicic Acid and even form brains of animals treated directly with CLA 17 , 18 , As such, CLA in cell culture demonstrated anti Aβ features and reduces p25 accumulation In this work, we have shown that long-term administration of Nano-PSO exerts a profound beneficial effect on 5XFAD mice 45 , significantly reducing their age-dependent cognitive decline.
To establish whether the mechanism of action of Nano-PSO in the AD model indeed results from inhibition of calpain activity, we looked into the levels of p25, the calpain product which binding to CDK5 results in deregulation of this important enzyme, eventually leading to neurodegeneration 46 , 47 , Interestingly, this was also true for the p25 levels in the brains of TgMHu2MEK mice.
This fact is particularly surprising since in these mice, while Nano-PSO exerts an intense beneficial clinical effect, it does not induce any reduction in the age depended accumulation of disease related PrP 28 , the mayor feature of prion diseases such as genetic CJD Most interestingly, p25, as opposed to the normal CDK5 activator p35 , is not readily degradable and tends to accumulate in brain of subjects suffering from neurodegenerative diseases This metabolic stability may be the cause for the deregulated activity of CDK5, eventually leading to neurodegeneration.
Whether the accumulation of p25 is the result or the cause of individual prion and prion like proteins accumulation remains to be established. The fact that long-term Nano-PSO administration decreases the levels of p25 in both AD and CJD animal models, concomitant with delay of clinical disease advance, reinforces the notion that brain targeted calpain inhibitors, in particular safe reagents that can be administered for long term periods, may be used as preventive treatments for an array of brain diseases.
Generation of self-emulsifying Nano-PSO is described in patent no. For drinking water preparation, Mice were allowed to drink freely from the diluted formula. We used 5XFAD mice 21 , 45 , 52 grown in our animal facility.
Mice comprising both transgenes were used for the experiments, while the non-Tg mice served as WT mice. All animal experiments were conducted under the guidelines and supervision of the Hebrew University Ethical Committee, which approved the methods employed in this project Permit Number: MD It was previously shown that there are no significant differences in cognitive performance tests between male and females in this transgenic line Water containers of all groups were replaced twice a week.
Mice were sacrificed several days after the completion of the cognitive test performed at 10 months of age and their brains collected and processed for immunohistochemistry and immunoblotting experiments.
The following cognitive tests were performed on two groups of either 5XFAD or C57B mice, at either 7 or 10 months of age. The results presented in this manuscript represent the average of the two groups.
The T maze test was use for assessing the spatial long-term memory, measuring exploratory behavior in animals, as described in Benharmon at all The number of entries to the unfamiliar arm and the time spent there were recorded. Normal healthy animals prefer to visit the new arm of the maze on the second day rather than the familiar arm.
The novel object recognition test is used to evaluate cognition, especially non-spatial recognition memory. The ratio of exploration of the novel object and the total exploration of the two objects were calculated and presented in the figure.
The test was performed using the Ethovision 10 system, providing fully computerized, blinded and unbiased measurement. Normal animals tent to explore the new object longer than the old one, indicating normally long-term recognition memory Twenty-four hours later, animals were re-exposed to the same environment.
Locomotion on the training and testing days were recorded using the Ethovision 10 system, providing fully computerized, blinded and unbiased measurement.
Bigger delta between days shorter distance on the test session compared to the training session represented intact learning Mice were sacrificed under anesthesia two hours after the administration of last dose. The filter paper was then rinsed with hot water until the filtrate was neutralized.
Previously extracted oil was placed in a distillation flask and 0. When the solution had reached boiling, BF 3 and Isooctane were added. The supernatant containing the fatty acid methyl ester FAME was collected and quantified by gas chromatograph, GC.
Bellefonete, PA, USA and flame ionization detector FID. Peaks were identified using Openlab software. Sections were stained for mouse α-human Aβ, clone α-6E10 and Thioflavin S sigma Aldrich to asses amyloid plaques, and with α COX IV-1 rabbit monoclonal antibody raised against a human COX IV-1 peptide which in mice recognizes only the COX IV-1 isomer for antibodies details see Supplementary Table 1.
Secondary antibodies coupled to Alexa Fluor and were purchased from Abcam. Nuclei were labeled with DAPI Fluoromount Vector Laboratories. Confocal analysis was performed by a Nikon A1R Confocal Laser Microscope System using the NIS-Elements C control software.
Membranes were then treated as described previously The 6E10 membrane was re-probed with α β-actin to examine the levels of total protein loaded onto the membrane.
Immunoreactive bands were analyzed using the ImageJ software. For antibodies details see Supplementary Table 1. Statistical analysis was performed using IBM SPSS Statistics V. Data was analyzed using either one-way ANOVA for OFH task and by contrast analysis for the T-maze and novel object recognition tests.
Statistical analysis for additional experiments pharmacokinetics, quantification of immunoblots and immunohistochemistry was done by t-test analysis.
These experiments were conducted under the guidelines and supervision of the Hebrew University Ethical Committee, which approved the methods employed in this project Permit Number: MD An amendment to this paper has been published and can be accessed via a link at the top of the paper.
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Article PubMed PubMed Central Google Scholar. Brown, K. The prion diseases. Article PubMed Google Scholar. Scheckel, C. Prions, prionoids and protein misfolding disorders.
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Inhibition of calpains improves memory and synaptic transmission in a mouse model of Alzheimer disease. Friedman-Levi, Y. Fatal prion disease in a mouse model of genetic EK Creutzfeldt-Jakob disease.
Keller, G. Other studies have shown similar results and that CLA also has no adverse effects on overall blood lipids, inflammation levels and insulin response in healthy, overweight and obese adults. One of the possible potential mechanisms by which CLA reduces body fat mass might be that it decreases energy intake or increases energy expenditure.
Does CLA reduce belly fat? The hypothesis is that CLA may be involved in insulin regulation. Conjugated lienoic acid has shown immune-enhancing effects and anticarcinogenic activities in several animal studies.
The CLA present in saturated-fat foods might offset the adverse effects of the saturated fat content and benefit everything from blood sugar control, to hormone regulation, to natural cancer prevention. Lower inflammation is a sign of less free radical damage or oxidative stress that is linked to lower cancer risk.
CLA seems to modulate immune and inflammatory responses as well as improve bone mass. Research on the effects of conjugated linoleic acid for preventing breast cancer is somewhat conflicting, but some early research suggests that higher intake of CLA from natural foods is linked with a lower risk of developing breast cancer.
Other study results suggest that it can be beneficial for fighting cancer of the digestive organs and can improve detoxification via healthier liver function , too.
Consuming foods high in CLA or taking CLA supplements for 12 weeks seems to improve symptoms and overall well-being in people with seasonal allergy symptoms. Similarly, some research shows that for people with asthma, CLA might be a natural treatment method for asthma-related symptoms, due to its ability to help control inflammation.
Twelve weeks of supplementation seems to improve airway sensitivity and ability to exercise. Early research suggests that CLA is beneficial for lowering inflammation and therefore autoimmune diseases like rheumatoid arthritis. Taking conjugated linoleic acid alone or along with other supplements like vitamin E benefits those with arthritis by reducing symptoms, including pain and morning stiffness.
Pain and inflammation markers including swelling have been improved for adults with arthritis taking CLA compared to their pre-treatment symptoms or people not taking CLA, meaning CLA can naturally treat arthritis.
Although findings have also been somewhat conflicting, some research shows that taking conjugated linoleic acid alone or along with supplements like creatine and whey protein can help increase strength and improve lean tissue mass.
This is why CLA is often added to some bodybuilding supplements, protein powders and weight loss formulas. According to a report published in The Journal of Food Composition and Analysis , the top food sources of CLA include :.
What an animal eats and the conditions in which they are was raised highly affect how much CLA and other fats or nutrients their meat or milk will supply. The proportion of CLA ranges from 0. In other words, not all beef or dairy is created equal when it comes to supplying us with healthy fats like CLA.
Even the season, quality of the soil on the farms and age of the animal affect the CLA content. One study, for example, found that the CLA content in beef and dairy from grass-fed cows is — percent higher compared to grain-fed cows.
Grass-fed beef contains higher levels of CLA and even more omega-3 fats and vitamins too than beef from factory farm-raised animals. The same goes for dairy products we get from cows, including cream or butter. Butter, beef and cream are nothing to be scared of, as long as you consume the highest quality you can, just like traditional populations have done for thousands of years.
Should you take CLA supplements? While CLA supplementation has shown some positive effects for managing risk and symptoms for some diseases, most might lack high levels of rumenic acid , which is the predominant form of CLA found in naturally occurring foods.
This comprises approximately 90 percent of CLA found in ruminant meats and dairy products and the most biologically active forms 9,11 and 10,12 isomers.
Functipn entails predominant pathological characteristics including amyloid beta Aβ CCLA formation, neurofibrillary entanglements, CLA and cognitive function brain atrophy, which gradually Metabolic syndrome hypertension in cognitive dysfunctions. Studies showed clgnitive these pathological changes are found in a functiob of brain structures, including the claustrum Funtion CLA and cognitive function, a nucleus Obesity and socioeconomic factors penetrates deeply into the brain and is extensively interconnected to various brain structures. The CLA modulates many aspects of cognitive functions, with attention, executive function, visuospatial ability, language, and memory in particular. It is also implicated in multiple neuropsychiatric disorders, of which one worthy of particular attention is AD-related cognitive impairments. To inspire novel AD treatment strategies, this review has summarized the CLA functionality in discriminative cognitive dysfunctions in AD. And then propose an array of potential mechanisms that might contribute to the cognitive impairments caused by an abnormal CLA physiology. Home injury prevention the Cooking skills for teens period Caffeine-free vitality booster neurodevelopment gestation and lactationan CLA and cognitive function of CLA and cognitive function fatty cognifive FAs can LCA the offspring cognitive function permanently causing damage. Lipids can regulate neurotrophin and compose cognitvie tissue. However, functlon effects fuction maternal consumption of a mixture of conjugated linoleic acid CLA on an offspring nervous system are not completely clear. We aimed to investigate the impacts of different CLA concentrations mixed into the maternal diet during early life on neonatal reflex maturation and cognitive functions of the offspring. After birth, the reflex responses of the offspring were observed from the 1st to the 21st day. The data were analyzed using one-way ANOVA and the Kruskal—Wallis test. CLA3 group explored less of the OF in the second exposure.
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