Brain Regions Of Aged Rats Research Articles

Effects of Atipamezole Preconditioning on Cognitive Function and Protein Expression in Related Brain Regions of Aged Rats after General Anesthesia.

To explore the possible mechanism of atipamezole in improving cognitive function after general anesthesia in aged rats, forty-five aged SD rats were separated into control, model, and atipamezole groups. Rats in the model group were anesthetized by intraperitoneal injection of 75 mg/kg ketamine plus 5 mg/kg midazolam. Results showed that the escape incubation period of the atipamezole group versus model group on the 2nd, 3rd, and 4th days was shortened, residence time of platform quadrant was prolonged on the 5th day, and number of times of crossing platform quadrant was increased. Compared with the control group, the residence time in the central region of the model group was shortened on the 1st, 2nd, and 3rd days. Atipamezole group's central residence time was prolonged on the 1st, 2nd, and 3rd days compared to the model group. Concentrations of IL-1, IL-6, and TNF-α in the hippocampus of the atipamezole group decreased significantly compared to the model group. The expressions of p-CREB and c-fos proteins in the prefrontal cortex and nucleus accumbens of rats in the atimezazole group were higher than those in the model group. In conclusion, atipamezole preconditioning can reduce cognitive dysfunction in aged rats after general anesthesia, and its mechanism may be related to inhibiting hippocampal inflammatory reaction and improving protein expression levels of p-CREB and c-fos in related brain regions of aged rats.

Age-related changes in CB1 receptor expression and function and the behavioral effects of cannabinoid receptor ligands

Cannabinoid use has increased among aging individuals. However, little information on age-related differences in the behavioral effects of these agents is available. To explore potential differences in the behavioral effects of cannabinoids, we determined effects of Δ9-tetrahydrocannabinol (THC, 1–10 mg/kg) or rimonabant (0.3–3.2 mg/kg) on operant fixed-ratio responding (FR10) for food in young adult (6 months) and aged (29 months) rats. THC dose-dependently decreased responding for food. Rimonabant alone had little or no effect on responding up to 1.0 mg/kg, but disrupted responding following a 3.2 mg/kg dose. Rimonabant (1.0 mg/kg) partially antagonized response disruption by THC. These effects were similar in young adult and aged rats. However, aging has been reported to change the neurobiology of cannabinoid CB1 receptors. To confirm our rats exhibited such differences, we assessed CB1 receptor binding sites and function in six subcortical (caudate, nucleus accumbens CA1, and CA2/CA3), and three cortical regions (medial prefrontal, temporal, entorhinal) in young adult (6 months) or aged (26 months) male Lewis rats using quantitative autoradiography. CB1 receptor binding sites were reduced in cortical, but not subcortical brain regions of aged rats. CB1 receptor function, at the level of receptor-G protein interaction, was not different in any region studied. Results indicate that down-regulation of CB1 receptor binding sites observed in cortical regions of aged rats was not accompanied by a commensurate decrease in CB1 receptor-stimulated [35S]GTPγS binding, suggesting a compensatory increase in receptor function in cortical areas. Together, our results provide additional evidence of age-related changes in central CB1 receptor populations. However, the functional compensation for decreased CB1 receptor binding may mitigate changes in behavioral effects of cannabinoids. With the rising use of cannabinoid-based therapeutics among aging populations, further evaluation of age-related changes in the cannabinoid system and the impact of these changes on effects of this class of drugs is warranted.

Maternal stress programs a demasculinization of glutamatergic transmission in stress-related brain regions of aged rats

Brain aging may be programmed by early-life stress. Aging affects males and females differently, but how perinatal stress (PRS) affects brain aging between sexes is unknown. We showed behavioral and neurobiological sex differences in non-stressed control rats that were strongly reduced or inverted in PRS rats. In particular, PRS decreased risk-taking behavior, spatial memory, exploratory behavior, and fine motor behavior in male aged rats. In contrast, female aged PRS rats displayed only increased risk-taking behavior and reduced exploratory behavior. PRS induced large reductions in the expression of glutamate receptors in the ventral and dorsal hippocampus and prefrontal cortex only in male rats. PRS also reduced the expression of synaptic vesicle-associated proteins, glucocorticoid receptors (GR), and mineralocorticoid receptors (MR) in the ventral hippocampus of aged male rats. In contrast, in female aged rats, PRS enhanced the expression of MRs and brain-derived neurotrophic factor (BDNF) in the ventral hippocampus and the expression of glial fibrillary acidic protein (GFAP) and BDNF in the prefrontal cortex. A common PRS effect in both sexes was a reduction in exploratory behavior and metabotropic glutamate (mGlu2/3) receptors in the ventral hippocampus and prefrontal cortex. A multidimensional analysis revealed that PRS induced a demasculinization profile in glutamate-related proteins in the ventral and dorsal hippocampus and prefrontal cortex, as well as a demasculinization profile of stress markers only in the dorsal hippocampus. In contrast, defeminization was observed only in the ventral hippocampus. Measurements of testosterone and 17-β-estradiol in the plasma and aromatase in the dorsal hippocampus were consistent with a demasculinizing action of PRS. These findings confirm that the brains of males and females differentially respond to PRS and aging suggesting that females might be more protected against early stress and age-related inflammation and neurodegeneration. Taken together, these results may contribute to understanding how early environmental factors shape vulnerability to brain aging in both sexes and may lay the groundwork for future studies aimed at identifying new treatment strategies to improve the quality of life of older individuals, which is of particular interest given that there is a high growth of aging in populations around the world.

Expression of vascular endothelial growth factor and microvessel density in different brain regions in aged rats

To observe the distribution of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in different brain regions in aged rats and determine the role of VEGF and MVD in the aging process of the nervous system. We observed the expression of VEGF and MVD in different parts of rat brain in the 3- month group and 30-month group with immunohistochemical technique. Compared with the 3-month group, the 30-month group showed fewer VEGF-positive cells and MVD in the brain (P<0.01), and the number varied significantly in different brain regions (P<0.01). The motor cortex region contained more VEGF-positive cells and MVD than the hippocampus and cerebellum. VEGF-positive cells and MVD are decreased in every brain region of aged rats, and the motor cortex region contains more positive cells, suggesting exogenous VEGF may enhance the formation of microvessels and delay the aging of the nervous system.

Effects of pregnenolone intervention on the cholinergic system and synaptic protein 1 in aged rats

Objective: To observe the effect of pregnenolone (PREG) intervention on the cholinergic system function and the synaptic protein 1 (SYP1) expression in different brain regions of aged rats. Method: Twenty-four-month-old male Sprague Dawley rats intraperitoneally injected every other day for one month were divided into blank control group, solvent control group, PREG (0.5 mg/kg) intervention group and PREG (2.0 mg/kg) intervention group. The rats were sacrificed 2 d after the intervention and the corresponding regions of brain tissue were separated and cryopreserved. Western blot analysis was used to detect the expression level of choline acetyltransferase (ChAT), SYP1, serum PREG and the activity of ChAT and acetylcholinesterase (AChE) in different brain regions. In addition, the semiquantitative changes in the expression level of ChAT and SYP1 in frontal lobe and hippocampus were tested by immunohistochemistry. Result: Western blot and immunohistochemistry analysis showed that PREG (2.0 mg/kg) administration led to a significant increase of ChAT and SYP1 expressions in frontal lobe, temporal lobe, and hippocampus regions (p < 0.05). The result of enzyme-linked immunosorbent assay showed that PREG (2.0 mg/kg) administration significantly increased ChAT activity and serum PREG levels and caused a decrease in AChE activity (p < 0.05); while PREG (0.5 mg/kg) only elevated levels of serum PREG. Conclusion: PREG significantly improved the synaptic plasticity of memory-related brain areas of aged rats, significantly increased brain cholinergic activity and thus helps to improve learning and memory in aged rats.

Effects of thyrotrophin-releasing hormone tartrate and its sustained release formulation on cerebral glucose metabolism in aged rats.

The effects of a sustained release formulation of thyrotrophin-releasing hormone (TRH) over two weeks (TRH-SR, 10 or 50 mg kg-1, equivalent to 0.56 or 2.80 mg kg-1 free TRH, respectively) and repeated treatment with TRH tartrate (TRH-T, 0.3, 1.0 or 3.0 mg kg-1, equivalent to 0.2, 0.7 or 2.0 mg kg-1 free TRH, respectively) on the rate of local cerebral glucose utilization (LCGU) were investigated using the quantitative autoradiographic 2-deoxy-[14C]D-glucose method in various brain regions of aged rats. In aged rats (28 months old), the LCGU was significantly reduced as compared with young adult rats (3 months old), while treatment with TRH-SR ameliorated the reduction of the LCGU in a dose-dependent manner. The brain regions ameliorated by TRH-SR were the auditory cortex, septal nucleus, substantia nigra, cerebellar cortex and cerebellar nucleus. In contrast, once-daily repeated treatment over one week with TRH-T at a dose of 0.3 mg kg-1 (equivalent to 50 mg kg-1 of TRH-SR) had no effect on the reduced LCGU in various brain regions in aged rats (27 months old), whereas treatment with a higher dose of TRH-T (0.7 or 2.0 mg kg-1 free TRH) significantly ameliorated the reduction. The comparison of the ameliorating potencies between TRH-T and TRH-SR indicated that TRH-SR had a potency about 7 times greater than TRH-T.

Expression of GLUT 3 in different brain regions of aged rats

To examine the distribution of glucose transport 3 (GLUT 3) in different brain regions of aged rats and to investigate its role in ageing process of the nervous system. The GLUT 3 expression in different brain regions was examined with immunohistochemical method in rats aged 3, 18 and 30 months, respectively. The number of GLUT 3-positive cells varied in the different brain regions in rats of all age groups (P<0.01); the CA1 region contained the greatest number of positive cells,and fewer in the motor cortex and cerebellum. The number of GLUT 3-positive cells was reduced in the brain of aged rats (P<0.01); and the neural cells in 4 different brain regions presented with large cell body and loose alignment. The expression of GLUT 3 decreased in aged rats, which suggests that GLUT 3 may be involved in the ageing process of nervous system.

Basal and hypercapnia-altered cerebrovascular perfusion predict mild cognitive impairment in aging rodents

With increasing age, a subset of otherwise healthy individuals undergoes impairments in learning and memory that have been termed mild cognitive impairment (MCI). The enhanced neuronal activity associated with learning and memory requires increased cerebral blood flow (CBF) to specific brain regions. However, the interactions between cerebral blood flow and MCI remain unclear. In this study, we address whether baseline or hypercapnia-induced (increased blood CO2 levels) changes in CBF are modified with age, and whether these measures are predictive of cognitive status in rodents. Adult and aged rats were evaluated using a hippocampally-dependent task in a water maze. Aged rats were classified as memory-impaired or memory-intact based on performance comparisons with adult rats. Cerebral blood flow was assessed using flow-alternating inversion recovery (FAIR) magnetic resonance imaging (MRI), before and after breathing 10% CO2. The transition period between CO2 concentrations was examined with blood oxygen level dependent (BOLD) MRI. Separation of aged animals into memory-intact and impaired categories revealed increased basal perfusion in the dorsal hippocampus of memory-impaired versus memory-intact aged animals. Linear regression revealed that higher hippocampal perfusion was correlated with impaired memory in aged animals, and a logistic regression indicated that hippocampal perfusion predicted spatial memory ability. Several brain regions of aged rats demonstrated an attenuation of the perfusion increase normally observed in adult rats under hypercapnia. Memory-impaired animals were the primary contributor to this effect, as their perfusion response to hypercapnia was significantly reduced compared to adult animals. Aged, memory-intact animals were not significantly different from adults. BOLD MRI demonstrated a reduced response in aged animals to hypercapnia, with impaired animals being the primary contributor to the effect. A logistic regression model based on basal and hypercapnia perfusion correctly predicted cognitive status in 83.3% of animals tested. Our results indicate that age-related changes in vascular reactivity and perfusion are important contributing factors in memory impairment.

Role of Glutathione monoester on age-related neurochemical alterations in rat brain

It is quite apparent that the incidence of neurodegenerative diseases in both men and women increases in a logarithmic fashion with age and begins to rise much more rapidly after the age of 60. Brain aging is accompanied by structural and functional changes at cellular and tissue levels such as increase in free radical generation, lowered antioxidant defenses, decrease in number of neurons, decrease in the activities of enzymes, (g) decrease in impulse transmission. The present study was aimed to assess the neuromodulatory role of Glutathione monoester (GME) when administered intraperitoneally (12mg/kg body weight) for 20 days on acetylcholine esterase (AchE) activity, levels of neurotransmitters such as dopamine, serotonin, norepinephrine and rotorod behavioral analysis in discrete brain regions of young and aged male albino Wistar rats. Age-related decrease (p<0.05) in acetylcholine esterase activity, neurotransmitter levels and also decrease in sensorimotor performance was observed. GME administration was effective in restoring these neuronal parameters in aged rat brain regions. Thus GME act as a neuromodulator in discrete brain regions of aged rats.

Modulatory Role of Glutathione Monoester in Augmenting Age-Associated Neuronal Antioxidant System

An ever-increasing number of reports show the involvement of free radicals in the functional and structural changes occurring in the brain as a part of the normal aging process. This study aimed to assess the potential efficacy of glutathione monoester (GME) when administered intraperitoneally (12 mg/kg body weight) for 20 days on memory and the antioxidant defense system and lipid peroxidation in discrete brain regions such as cortex, striatum, and hippocampus of young and aged rats. Age-associated decline in memory and activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione, vitamin E, and vitamin C, and elevated levels of lipid peroxidation and oxidized glutathione, were observed in all the brain regions studied (p < .001). GME administration was effective in restoring the antioxidant status and in decreasing lipid peroxidation level in aged rat brain regions.

Nicotine-induced fibroblast growth factor-2 restores the age-related decline of precursor cell proliferation in the subventricular zone of rat brain

Precursor cell proliferation is present in the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) of the dentate gyrus of the hippocampus of adult rat and persists during aging although at reduced levels. Previous studies have shown that acute intermittent nicotine treatment significantly increases fibroblast growth factor-2 (FGF-2) expression in several brain regions of aged rats. The aim of the present investigation was to test the hypothesis that nicotine-induced expression of FGF-2 may restore the age-related decline of precursor cell proliferation. It was first demonstrated that nicotine treatment increases both mRNA and protein FGF-2 in the SVZ of aged male rats (18 months old). The effect of nicotine on precursor cell proliferation in the SVZ was studied by i.p. injection of 5-bromo-2′-deoxyuridine (BrdU) 40 mg/kg to label dividing cells. The nicotine treatment was found to significantly enhance precursor cell proliferation in the SVZ. This increase was sufficiently large to restore the age-related decline of proliferating precursor cells observed in aged rats to that found in young adult rats (3 months old). FGF-2 was expressed in GFAP-positive cells and may act via its receptor FGFR1 that was found expressed in nestin-positive cells of the SVZ. The data obtained demonstrated that the age-related decline of precursor cell proliferation may be counteracted by activating a trophic mechanism mediated by FGF-2.

Protective Efficacy of α-Lipoic Acid on Acetylcholinesterase Activity in Aged Rat Brain Regions

The purpose of the present investigation was to measure the activity of acetylcholinesterase in discrete regions of young and aged rat brain before and after DL-alpha-lipoic acid supplementation. Two groups of male albino rats were used in this study (4 and 24 months of age). DL-alpha-lipoic acid was administered intraperitoneally with a regimen of 100 mg/kg body weight per day using alkaline saline as a vehicle for 7 and 14 days. The activity was measured in the cerebral cortex, cerebellum, striatum, hippocampus and hypothalamus, and found to be significantly decreased in some of the brain regions in aged rats. Administration of lipoic acid into aged rats reversed the decrease in the activity in the discrete brain regions. These results suggest that lipoic acid is effective in restoration of the activity of acetylcholinesterase in aged rats.

Neuroprotective and Anti-ageing Effects of Curcumin in Aged Rat Brain Regions

This study investigated the influence of chronically administered curcumin on normal ageing-related parameters: lipid peroxidation, lipofuscin concentration and intraneuronal lipofuscin accumulation, activities of the enzymes superoxide dismutase (SOD), glutathione peroxidase (GPx), and Na(+), K(+), -adenosine triphosphatase (Na(+), K(+), -ATPase) in different brain regions (cerebral cortex, hippocampus, cerebellum and medulla) of 6- and 24-month-old rats. In normal ageing, lipid peroxidation and lipofuscin concentration were found to increase with ageing, the activities of SOD, GPx and Na(+), K(+), -ATPase, however, decreased with ageing. Chronic curcumin treatment of both 6 and 24 months old rats resulted in significant decreases in lipid peroxide and the lipofuscin contents in brain regions, the activities of SOD, GPx and Na(+), K(+), -ATPase however, showed significant increase in various brain regions. The present study, thus, demonstrated the antioxidative, antilipofusinogenesic and anti-ageing effects of curcumin in the brain.

Oxidative stress-mediated macromolecular damage and dwindle in antioxidant status in aged rat brain regions: Role of l-carnitine and dl-α-lipoic acid

Background The free radical theory of aging has significant relevance in a number of age-related neurological disorders. Too many free radicals create cellular pollution that shuts down energy levels. They have also been implicated in the loss of physiological functioning associated with the aging of post mitotic cells such as the brain. The activities of enzymatic antioxidative defenses decrease in rat brain may be possible causes of age-associated increase in oxidative damage to macromolecules. Methods We determined whether dl-α-lipoic acid (100 mg/kg body weight/day), and l-carnitine (300 mg/kg body weight/day) together when administered for 30 days declines the rate of oxidative stress-mediated macromolecular damages such as lipid peroxidation (LPO), protein carbonyl (PCO) and DNA protein cross-links in different anatomic regions (cortex, striatum and hippocampus). The activities of antioxidant enzymes in programmed aging were evaluated in the cortex, striatum and hippocampus of young and aged rat brain regions. Results Aged rats elicited a significant decline in the antioxidant status and increase in LPO, PCO and DNA protein cross-links as compared to young rats in all the 3 brain regions. The increase in LPO, PCO and DNA protein cross-links were (35.8%, 35.6%, 43.5%) in cortex, (32.5%, 40.3%, 29.8%) in striatum and (62.7%, 42.4%, 34.9%) in hippocampus, respectively, in aged rats as compared to young rats. Co-supplementation of carnitine and lipoic acid was found to be effective in reducing brain regional LPO, PCO and DNA protein cross-links and in increasing the activities of enzymatic antioxidants in aged rats to near normalcy. Conclusion The combination of l-carnitine and lipoic acid overcame the oxidative stress induced rate of lipid peroxidation, protein carbonyl formation, accumulation of DNA protein cross-links and deficits in antioxidant enzyme activities in various brain regions of aged rats.

Alpha-lipoic acid increases Na+K+ATPase activity and reduces lipofuscin accumulation in discrete brain regions of aged rats.

A convincing link between oxidative stress and neurodegenerative diseases has been found with the knowledge that it actually damages neuronal cells in culture. We analyzed the effect of DL-alpha-lipoic acid on lipofuscin and Na(+)K(+) ATPase in discrete brain regions of young and aged rats. In aged rats, the level of lipofuscin was increased, and the activity of Na(+)K(+)ATPase was decreased. Intraperitoneal administration of lipoic acid to aged rats led to a duration-dependent reduction and elevation in lipofuscin and enzyme activity, respectively, in the cortex, cerebellum, striatum, hippocampus, and hypothalamus of the brain. These results suggest that lipoic acid, a natural metabolic antioxidant, should be useful as a therapeutic tool in preventing neuronal dysfunction in aged individuals.

Age-dependent alterations in mitochondrial enzymes in cortex, striatum and hippocampus of rat brain ? potential role of L-Carnitine

Mitochondria link the energy -- releasing activities of electron transport and proton pumping with the energy conserving process of oxidative phosphorylation to form ATP. A declined mitochondrial performance has been generally observed during aging. In the present investigation, the activities of tricarboxylic acid cycle enzymes such as isocitrate, alpha-ketoglutarate, succinate and malate dehydrogenases and electron transport complexes I-IV were measured in mitochondria isolated from brain regions like cortex, striatum and hippocampus of young and aged rats before and after L-Carnitine supplementation. All the three brain regions of aged rats showed decreased activities of isocitrate, alpha-ketoglutarate and succinate dehydrogenases, complexes I and IV when compared to control young rats. Striatum seems to be the most susceptible region when compared to hippocampus and cortex. L-Carnitine supplementation to aged rats reversed the activities of these enzymes to near normal whereas treatment to young rats did not show any significant alterations. These results confirm that L-Carnitine can alleviate the age-associated decline in the metabolic efficiency of mitochondria in all three brain regions under investigation.

Neurostimulatory and antioxidative effects of L-deprenyl in aged rat brain regions.

This study investigated the influence of chronically administered L-deprenyl on normal ageing-related parameters: multiple unit action potentials, the activities of the enzymes Na(+),K(+)-adenosine triphosphatase, glutathione-s-transferase and glutathione peroxidase, and the levels of lipid peroxidation products and lipofuscin contents in the brain regions (cerebral cortex, hippocampus, striatum and thalamus) of 24-month-old rats. The drug increased the activity of Na(+),K(+)-ATPase and glutathione-s-transferase. The activity of glutathione peroxidase remained unaffected. The drug also increased the multiple unit action potentials activity. The levels of lipid peroxidation products were, however, decreased, and lipofuscin accumulation was diminished by the drug. The results essentially indicated that chronic treatment of rats with L-deprenyl significantly influenced the ageing-related alterations in: multiple unit action potentials, Na(+),K(+)-adenosine triphosphatase, glutathione-s-transferase, lipid peroxidation products and lipofuscin accumulation. These novel data on the effect of L-deprenyl on parameters of normal ageing provide new additional evidence concerning the anti-ageing therapeutic potential of L-deprenyl.

Effect of DL-α-lipoic acid on the status of lipid peroxidation and protein oxidation in various brain regions of aged rats

Free radicals have been implicated in the development of many acute and chronic diseases and in conditions involving brain or neurological tissue. The primary genetic material is subjected to damage by endogenous and exogenous agents, which may lead to instability and transcriptional infidelity. In the present study, we evaluated the protective effect of DL-α-lipoic acid, a metabolic antioxidant on lipid peroxidation, protein carbonyl content in various brain regions of aged rats when compared to brain regions of young rats. DL-α-lipoic acid was administered intraperitoneally (100mg/kg body weight/day) to experimental rats. Nucleic acid and protein content were low whereas thiobarbituric acid reactive substances and protein carbonyl content (markers of free radical damage) were high in cortex, striatum, hippocampus and hypothalamus followed by cerebellum of aged rat brain. Lipoate administration for 14 days in aged rats increased the levels of nucleic acid and protein and reduced lipid peroxidation and protein oxidation. These results demonstrate that lipoic acid is a potent antioxidant for neuronal cells against age associated oxidative damage.

Effect of DL-α-lipoic acid on the status of lipid peroxidation and antioxidant enzymes in various brain regions of aged rats

The effect of DL-α-lipoic acid on lipid peroxidation and antioxidant enzymes were evaluated in various brain regions of young and aged rats. Lipoate contents of discrete brain regions were also measured. In aged rats, the activities of superoxide dismutase, glutathione peroxidase, glutathione reductase and glucose-6-phosphate dehydrogenase were low whereas thiobarbituric acid reactive substances were found to be high. Catalase activity in various brain regions was little altered in aged rats. Lipoic acid an antioxidant was administered intraperitoneally (100mg/kg body weight per day) for 7 and 14 days. Lipoate administered aged rats showed a duration dependent reduction in the level of lipid peroxidation and elevation in the activities of antioxidant enzymes. There was a rise in the level of lipoate in aged rats after supplementation of lipoate in all the brain regions examined. From our results we conclude that lipoate supplementation had a beneficial effect in both preventing and reversing abnormalities in ageing brain. This beneficial effect was associated with normalization of lipid peroxidation and partial restoration in the activities of various enzymatic antioxidants suggesting that lipoate supplementation could improve brain antioxidant functions in the elderly.

Acetyl- l-carnitine enhances Na +, K +-ATPase glutathione- s-transferase and multiple unit activity and reduces lipid peroxidation and lipofuscin concentration in aged rat brain regions

This study investigated the effects of chronically administered acetyl- l-carnitine (ALC) on sodium potassium adenosine triphosphatase (Na +, K +-ATPase), glutathione- s-transferase (GST), glutathione peroxidase (GPx), multiple unit activity (MUA) and lipid peroxidation (LP) and lipofuscin (LF) concentration in brain regions: cerebral cortex, hippocampus, striatum and thalamus, of 24-month-old rats. The activity of Na +, K +-ATPase and GST was enhanced; that of GPx was unaffected. The MUA was increased while the levels of LP and LF were decreased. These novel data provide new additional evidence concerning the antiaging attributes of ALC.