Calorie restriction modulates neuro-immune system differently in young and aged rats.

Aging weakens and deregulates the immune system and plays an impact on the central nervous system (CNS). A crosstalk in between the CNS-mediated immune system and the body's overall innate immunity is often found to increase and subsequently accelerate neurodegeneration and behavioural impairment during aging. Dietary calorie restriction (CR) is found to be a beneficial non-invasive anti-aging therapy as it shows rejuvenation of stress response, brain functions and behaviour during aging.

Carnosine improves aging-induced cognitive impairment and brain regional neurodegeneration in relation to the neuropathological alterations in the secondary structure of amyloid beta (Aβ).

Aging-induced proteinopathies, including deterioration of amyloid beta (Aβ) conformation, are associated with reductions in endogenous levels of carnosine and cognitive impairments. Carnosine is a well-known endogenous antioxidant, which counteracts aging-induced Aβ plaque formation. The aim of this study was to investigate the effects of exogenous carnosine treatments on aging-induced changes (a) in the steady-state level of endogenous carnosine and conformation of Aβ secondary structure in the different brain regions (cerebral cortex, hippocampus, hypothalamus, pons-medulla, and cerebellum) and (b) cognitive function.

Metabolic disorder in Alzheimer's disease.

Alzheimer's disease (AD), a well known aging-induced neurodegenerative disease is related to amyloid proteinopathy. This proteinopathy occurs due to abnormalities in protein folding, structure and thereby its function in cells. The root cause of such kind of proteinopathy and its related neurodegeneration is a disorder in metabolism, rather metabolomics of the major as well as minor nutrients.

Carnosine research in relation to aging brain and neurodegeneration: A blessing for geriatrics and their neuronal disorders.

Carnosine, an endogenous dipeptide (β-Ala-l-His), is enriched in prefrontal cortex and olfactory bulb of the brain, blood and also in muscle. It has mainly antioxidant and antiglycating properties which makes this molecule unique. Its content reduces during aging and aging-induced neurodegenerative diseases.

Calorie restriction improves aging-induced impairment of cognitive function in relation to deregulation of corticosterone status and brain regional GABA system.

Aging is known to affect adversely the corticosterone status and the brain function including cognition. Calorie restricted (CR) diet has been found to improve brain aging. The objective of the present investigation is to study the effect of short-term CR diet without any food deprivation on aging-induced impairment of cognitive function in relation to the corticosterone status and the brain regional GABA system.

Does patchouli oil change blood platelet monoamine oxidase-A activity of adult mammals?

Patchouli oil, an essential aroma oil extracted from patchouli leaf during short-term exposure with five and ten drops either inhibited (at 1 or 2 h) or stimulated (at 4 h) the platelet MAO-A activity depending on the dosages of the aroma oil mainly due to inhibition or stimulation of its K . The long-term 15 consecutive days exposure (with two or five drops) of patchouli oil, on the other hand, maximally stimulated the platelet MAO-A activity with five drops patchouli oil for 1 h exposure, but further continuation of its exposure with same doses (two or five drops) for 30 consecutive days significantly stimulated (with two drops) and inhibited (with five drops) the platelet MAO-A activity due to stimulation and inhibition respectively of its corresponding both K and V . These results thus suggest that this aroma oil exposure may modulate the blood platelet serotonergic regulation depending on the dose, duration, and conditions of exposure.

Carnosine reverses the aging-induced down regulation of brain regional serotonergic system.

The purpose of the present investigation was to study the role of carnosine, an endogenous dipeptide biomolecule, on brain regional (cerebral cortex, hippocampus, hypothalamus and pons-medulla) serotonergic system during aging. Results showed an aging-induced brain region specific significant (a) increase in Trp (except cerebral cortex) and their 5-HIAA steady state level with an increase in their 5-HIAA accumulation and declination, (b) decrease in their both 5-HT steady state level and 5-HT accumulation (except cerebral cortex). A significant decrease in brain regional 5-HT/Trp ratio (except cerebral cortex) and increase in 5-HIAA/5-HT ratio were also observed during aging.

Carnosine: effect on aging-induced increase in brain regional monoamine oxidase-A activity.

Aging is a natural biological process associated with several neurological disorders along with the biochemical changes in brain. Aim of the present investigation is to study the effect of carnosine (0.5-2.

Involvement of high plasma corticosterone status and activation of brain regional serotonin metabolism in long-term erythrosine-induced rearing motor hyper activity in young adult male rats.

Long-term consumption of artificial food color(s) can induce behavioral hyperactivity in human and experimental animals, but no neurobiochemical mechanism is defined. This study investigates the role of brain regional serotonin metabolism including its turnover, MAO-A activity, and plasma corticosterone status in relation to behavioral disturbances due to an artificial food color, erythrosine. Long-term (15 or 30 consecutive days) erythrosine administration with higher dosage (10 or 100 mg/kg/day, p.

Short-term erythrosine B-induced inhibition of the brain regional serotonergic activity suppresses motor activity (exploratory behavior) of young adult mammals.

Previous studies showed that repeated ingestion of erythrosine B (artificial food color) developed behavioral hyperactivity, but nothing is known about its single administration effect as well as the neurochemical (s) involvement. The present study provides evidence that a single higher dosage (10, 100 or 200 mg/kg, p.o.

Long-term caffeine consumption reverses tumor-induced suppression of the innate immune response in adult mice.

Caffeine (1,3,7-trimethylxanthine), the active principle alkaloid of coffee ( Coffea arabica) and tea ( Camellia sinensis) possesses a restraining effect on tumor-induced suppression of the specific immune response in adult mice. The present study deals with the effect of long-term consumption of caffeine in the development of Ehrlich ascites carcinoma (EAC) cells in adult Swiss female mice, in relation to the innate immune response and tumor growth. Although the consumption of caffeine alone for more than 12 consecutive days did not affect the innate immune response parameters, continuation of its treatment following intraperitoneal EAC cell inoculation not only reduced the IN VIVO tumor growth but also reduced/restored the EAC cell-induced suppression of the innate immune response.

Dietary protein-carbohydrate ratio: exogenous modulator of immune response with age.

Manipulation of dietary variables is one the most described events to retard the aging process and maintain immune function. The present study deals with the effect of variable dietary protein-carbohydrate ratios (without caloric restriction) on the alteration of immune response of male albino rats at the level of lymphocyte viability, proliferation, cytotoxicity, DNA fragmentation of blood, spleen and thymus and corticosterone levels in plasma and adrenal gland in relation to aging and duration of dietary exposure. Young (3 months) and aged rats (18 months) maintained with control diet [protein (20%)-carbohydrate (68%)] showed age-induced decrease in immune response with an increase in plasma corticosterone level.

Long-term exposure of variable dietary protein-to-carbohydrate ratio: effect on brain regional glutamatergic activity with age.

Glutamatergic activity of hypothalamus and hippocampus of young (3 months) male albino rats having normal diet [protein (20%)-carbohydrate (68%)] was increased with the increase of age. Long-term (60 consecutive days) feeding of low protein (8%)-high carbohydrate (80%) diet (LP-HC) increased glutamatergic activity in these brain regions of young rats and decreased that in aged (18 months). On the contrary, supplementation of high protein (50%)-low carbohydrate (38%) diet (HP-LC) under similar condition decreased glutamatergic activity in those brain regions of young and increased that in aged brain regions.

Does caffeine reverse the EAC cell-induced immune suppression?

The aim of this study was to investigate the effect of long-term consumption of caffeine in the development of Ehrlich ascites carcinoma (EAC) cells in adult female mice, 25-30 g, in relation to immune response. Mice were treated with caffeine (20 mgkg(-1) daily, p.o.

Long-term caffeine-induced inhibition of EAC cell progression in relation to gonadal hormonal status.

Inhibitory action of caffeine (a tri-methylxanthine alkaloid) on progression or pathogenesis of lung, breast and ovarian cancer including Ehrlich ascites carcinoma (EAC) cell development has been reported. This information led the authors to study the effect of long-term administration of caffeine (20 mg/kg/day; po for 22-27 consecutive days) on the development of EAC cells in relation to serum gonadal hormones (LH, FSH, 17-OH-beta-estradiol (E2) and progesterone) in adult Swiss albino female mice. Measurement of gonadal hormones in serum using RIA showed that (a) long-term caffeine treatment significantly increased LH (except for 27 consecutive days) and decreased FSH (except for 24 and 27 consecutive days) and both E2 and progesterone (except for 22 and 24 consecutive days) levels, (b) development of EAC cell for 10-15 days, significantly increased LH but decreased FSH, E2 and progesterone levels and (c) long-term caffeine consumption during the development of EAC cell (i) restored the EAC cell- or caffeine-induced induction of LH and reduction of FSH level to their normal levels and (ii) withdrew/reduced the EAC cell-induced reduction in only E2 but not progesterone level.

Dietary variation of protein-carbohydrate: effect on hypothalamic and hippocampal GABA-glutamate in relation to aging.

Dietary protein variation has been found to alter brain regional neurochemistry with aging. In the present investigation, we studied the effect of short-term treatment of protein-carbohydrate variable diet to rat on hypothalamic and hippocampal gamma-amino butyric acid (GABA)-glutamate metabolism with increase of age. Exposure of male albino rats with diet containing normal protein (20%)-normal carbohydrate (68%) increased GABA metabolism and decreased glutamate metabolism in both hypothalamus and hippocampus with the increase of age.

Chronic administration of caffeine: effect on the activities of hepatic antioxidant enzymes of Ehrlich ascites tumor-bearing mice.

Chronic ingestion (for 22-30 consecutive days) of caffeine (20 mg/kg/day, p.o.) increased the activities of the hepatic enzymes- catalase (CAT) and superoxide dismutase (SOD) and decreased its lipid peroxidation (LP) in mice.

Brain regional gamma-aminobutyric acid (GABA) and locomotor activity: effect of long-term aldrin exposure.

Aldrin-induced stimulation of locomotor activity (LA) under nontolerant conditions was restored to control value after 20 or more consecutive days of aldrin administration. In contrast to the inhibition of GABAergic activity with aldrin under short-term conditions as observed in our previous study, the measurement of steady-state level of GABA, the activities of its metabolizing enzymes, turnover and the specific binding of GABA to its receptor in different regions of the brain of rats treated with aldrin (2 or 5 mg/kg/day, po) under long-term (for 30 consecutive days) conditions showed no change in the GABAergic activity in any regions of the rat brain. Moreover, the studies of the interaction between neurotransmitters (using agonist(s) and antagonist(s) of the respective neurotransmitter receptors) showed that long-term administration of aldrin restored the LA to control value by upregulation of central GABAergic activity through the interaction with dopaminergic and cholinergic systems.