Mood Cancer Research Results
Mood, Behaviour: Click to Expand ⟱
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Mood, including calmness vs aggression
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Scientific Papers found: Click to Expand⟱
*cognitive↑, Vitamin B12 deficiency causes treatable dementia and vitamin B12 supplementation has been reported to improve cognitive function
*memory↑, Kobe et al. reported that low vitamin B12 concentration within the normal range is poorer memory performance which is an effect that is partially mediated by hippocampal microsurgical integrity examined by MRI
*Mood↑, The improvement in cognitive function may have been associated with improvement in mood disorders, at least in part
*Risk↓, There is evidence that damage or dysfunction of the 5-HT system contributes to the development of AD, and different subtypes of 5-HT receptors are a potential target for the treatment of AD
*5HT↓, Serotonin is an antioxidant that inhibits the generation of ROS, malondialdehyde and carbonyls, prevents thiol oxidation, reduces the degradation of 2-deoxy-D-ribose, and prevents apoptosis
*ROS↓,
*MDA↓,
*Apoptosis↓,
*Mood↑, Serotonin deficiency may be responsible for the increase in aggressive behavior and depression often observed in patients with AD.
*other↑, Exercise and a Mediterranean diet increase 5-HT and BDNF levels, thereby improving mood and cognition.
*other↑, In particular, the evidence suggests that sulforaphane’s beneficial effects can be mainly ascribed to its peculiar ability to activate the Nrf2/ARE pathway [271].
*5HT↑, Moreover, the 5-HTP group showed a significant increase in serum serotonin levels.
*cognitive↑, 5-HTP supplementation can enhance cognitive performance and reduce symptoms of depression in Singaporean older adults, potentially through serotonergic modulation.
*BBB↑, 5-HTP could cross the blood-brain barrier and synthesize serotonin, thereby effectively elevating serotonin levels
*Mood↑, Prior studies have also observed the effect of 5-HTP on mood regulation, especially improvements in patients with depression
*antiOx↑, Blueberries contain polyphenolic compounds, most prominently anthocyanins, which have antioxidant and anti-inflammatory effects.
*Inflam↓,
*memory↑, anthocyanins have been associated with increased neuronal signaling in brain centers mediating memory function as well as improved glucose disposal, benefits that would be expected to mitigate neurodegeneration.
*neuroP↑, preliminary study suggest that moderate-term blueberry supplementation can confer neurocognitive benefit
*cognitive↑, At 12 weeks, we observed improved paired associate learning (p = 0.009) and word list recall (p = 0.04).
*Mood↑, In addition, there were trends suggesting reduced depressive symptoms (p = 0.08) and lower glucose levels (p = 0.10)
*glucose↓,
*antiOx↑, potent antioxidant and has been shown to exhibit anti-inflammatory, antitumorigenic and antimicrobial activities
*Inflam↓,
*BBB↑, Its ability to cross the blood–brain barrier is important as it contributes to its pharmacological activity against neurological disorders
*5HT↑, Apigenin improved serotonin, dopamine and epinephrine levels, which were altered in depressive animals
*CREB↑, Apigenin further regulates the cAMP-CREB-BDNF signalling pathway and N-methyl-D-aspartate (NMDA) receptors, which play important roles in neuronal survival, synaptic plasticity, cognitive function and mood behaviour
*BDNF↑, Apigenin improved BDNF levels and enhanced ERK1/2 and CREB expression
*memory↑, All the studies showed that apigenin improved learning and memory, except for two studies.
*motorD↑, In the open field test, apigenin improved locomotor activity
*Mood↑, The splash test revealed that apigenin improved grooming activity and locomotion in streptozotocin-induced depressive-like behaviour in a mouse model via an improvement in grooming activity.
*cognitive↑, The studies included in this systematic review showed that apigenin improved cognitive function and neurobehaviour in impaired or stressed animals.
*ROS↓, inhibition of ROS production
*BChE↓, Essential oils (EOs) from Salvia leriifolia Benth. exhibited high BChE inhibitory.
*AChE↓, Volatile oil from Marlierea racemosa Vell. (Myrtaceae) demonstrated concentration‐dependent inhibition of AChE
*other↓, EOs from the leaves and flowers of Polygonum hydropiper L., 28 sandalwood oil and its chief constituent α‐santalol were reported the AChE, BChE inhibitory efficacy.
*other?, The extract of Rosmarinus officinalis L. leaf led to improved long‐term memory in scopolamine‐induced rats, which can be partially explained by its inhibition of AChE activity in rat brain
*Ach?, It was observed in APP/PS1 mice that 4 weeks of Lemon essential oil treatment could significantly decrease hippocampal AChE, and thus increased ACh levels
*eff↑, Most studies have found that terpenoids in aromatic plant extracts are the main anticholinesterase active components
*antiOx↑, aromatic plant extracts for their potent antioxident and free radical scavenging properties
*ROS↓, Several compounds like safranal, linalool, and SHXW essential oil have been found to decrease ROS levels induced by Aβ in rats or mouse
*cognitive↑, aromatic plant extracts can improve cognitive function, reduce agitation, and improve sleep quality in AD patients.
*Mood↑,
*Sleep↑,
*QoL↑, Some studies reported that aromatherapy significantly improved the QoL of PWD and relieved the distress and burden of caregivers, promoted a positive experience among caregivers
*Mood↑,
*cognitive↑, EOs were effective on several pathological targets and have improved cognitive performance in animal models and human subjects.
*AChE↓, Recently, Ayaz et al. (2015) reported the AChE, BChE inhibitory and free radicals scavenging efficacy of EOs from the leaves and flowers of Polygonum hydropiper.
*BChE↓,
*ROS↓,
*other↓, , Ahmad et al. (2016) reported the anti-cholinesterase and antiradicals potentials of EO from Rumex hastatus D. Don. GC-MS analysis of EO revealed the presence of 123 compounds. I
*other↓, (Ahmad et al., 2016). Okello et al. (2008) reported the in vitro AChE, BChE inhibitory activity of flower oil from Narcissus poeticus L. belonging to family Amaryllidaceae.
*other↓, The EO from Marlierea racemosa Vell. (Myrtaceae) were evaluated by Souza et al. (2009) against AChE enzyme.
*other↓, C. salvifolius exhibited AChE inhibitory activity with IC50 value of 58.1 μg/ml. Whereas, C. libanotis, C. creticus and C. salvifolius showed significant inhibitory activities against BChE with IC50 values of 23.7, 29.1 and 34.2 μg/ml respectively.
*other↓, Rosemary EO also possess moderate AChE inhibitory activity and can synergistically act with 2-pinene and 1,8-cineole.
*memory↑, Owing to the memory enhancing capabilities of Salvia lavandulifolia Vahl (Spanish sage),
*BACE↓, EOs can inhibit the activity of BACE1 to hamper the Aβ load.
*Mood↑, Lavandula angustifolia Mill. and Melissa officinalis L. belonging to Lamiaceae for the management of agitation in individuals with severe dementia. The sedative and calming effect of both EOs is already established which can contribute in consolidati
*motorD↑, lavender EO: locomotor activity and motor functions were improved in animal models.
*Mood↑, All of these studies demonstrated a significant impact on behavioural problems in patients with dementia, with negligible side-effects.
*GABA↑, GABA augmentation
*Sleep↑, ambient lavender oil was as effective in controlling poor sleep patterns
*Mood↑, therapy massage with lavender oil showed a significant improvement in behaviour in the hour after treatment.
*cognitive↑, The most notable cognitive and mood effects were improved memory performance and increased 'calmness' at all postdose time points for the highest (1600 mg) dose.
*memory↑,
*AChE∅, However, no cholinesterase inhibitory properties were detected
*Mood↑,
*eff↝, The results also suggest that different preparations derived from the same plant species may exhibit different properties depending on the process used for the sample preparation.
*memory↑, Current evidence suggests that lemon balm may be effective in improving anxiety and depressive symptoms, particularly in the acute setting.
*Mood↑,
*Mood↑, Lemon Balm more effective in reducing NPI agitation
*memory↑, Lavender more effective in reducing CMAI PNAB (p = 0.04) in dementia.
*Mood↑, WMO and RA significantly reduced depressive-like behavior
*antiOx↑, Berberine has multiple therapeutic actions, including antioxidant, anti‐inflammatory, antitumour, antimicrobial, hepatoprotective, hypolipidemic, and hypoglycemic actions.
*Inflam↓,
*hepatoP↑,
*eff↑, recent studies show that berberine has a protective effect on central nervous system disorders, such as Alzheimer's, cerebral ischaemia, mental depression, schizophrenia, and anxiety
*5HT↑, Chronic administration of berberine (5 mg/kg, ip) for 15 days significantly increased the levels of norepinephrine (29%), serotonin (19%) as well as dopamine (52%)
*Mood↑, An antidepressant effect of berberine results from elevation of brain‐derived neurotrophic factor (BDNF) levels.
*BDNF↑,
*cognitive↑, Caffeine has cognitive‐enhancing properties with effects on learning and memory, concentration, arousal and mood
*memory↑,
*Mood↑,
*BDNF↑, caffeine induces massive secretion of BDNF in cultured hippocampal neurons
*TrkB↑, These observations strongly suggest that TrkB activation is involved in CAFLTP.
*Inflam↓, Active components such as Phenol, Cinnamaldehyde, Turmerone, Proanthocyanidin and Linalool as well as Eugenol can provide antidepressant effects through anti- inflammatory prevention.
*BDNF↑, Cinnamaldehyde will be metabolized in the body and produce a metabolite, namely NaB (Sodium Benzoate Metabolite) which can increase BDNF (Brain-derived neurotrophic factor)
*TNF-α↓, cinnamon extract inhibited the action of the pro-inflammatory cytokine TNF-α in the brain hippocampus
*lipid-P↓, Cinnamon also has active substances such as Linalool and Eugenol. Both of these active substances have the function of reducing the oxidation of lipids.
*Mood↑, active ingredient components
contained in cinnamon have anti-depressant effects
which can be used as an alternative treatment for
depressed patients
*BBB↑, 17 components had a good absorption due to the blood–brain barrier (BBB) limitation;
*GABA↑, further clustering analysis of active ingredient targets by network pharmacology showed that the GABA pathway with GABRG2 as the core target was significantly enriched;
*eff↑, we screened five components, methyl cinnamate, propyl cinnamate, ( +)-procyanidin B2, procyanidin B1, and myristicin as the brain synapse-targeting active substances of cinnamon
*antiOx↑, Cinnamon is multi-targeted and multi-effective and is widely used in treating AD because of its antioxidant, anti-inflammatory, antibacterial, anti-anxiety and antidepressant properties
*Inflam↑,
*Mood↑,
*CREB↑, 25 and 50 mg/kg of crocin increased the levels of CREB and BDNF significantly and dose dependently.
*BDNF↑,
*Mood↑, crocin has antidepressant-like action by increasing CREB, BDNF and VGF levels in hippocampus
*BDNF↑, treatment of curcumin increased BDNF and phosphor-TrkB
*TrkB↑,
*CREB↑, curcumin-induced increase in phosphorylated cyclic AMP response element binding protein (CREB), which has been implicated as a possible mediator of antidepressant actions
*Mood↑,
*neuroP↑, Therefore, we hypothesize the neuroprotection of curcumin might be mediated via BDNF/TrkB-MAPK/PI-3K-CREB signaling pathway.
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*Mood↑, The current study indicates that Ellagic acid intervention has a favorable effect on depression in MS patients.
*BDNF↑, we found a significant elevation in circulating levels of BDNF and serotonin.
*5HT↑,
*antiOx↑, associated to its antioxidative, anti-inflammatory, immunomodulatory, antidiabetic, and anticancer properties (Gupta et al., 2021)
*Inflam↓,
*AntiCan↑,
*QoL↑, Ellagic acid improves bowel function and enhances the quality of life for individuals suffering from irritable bowel syndrome (IBS)
*neuroP↑, Ellagic acid may have neuroprotective effect by regulating the hypothalamic–pituitary–adrenal (HPA) axis and neurotransmitters in animal's brain
*cognitive↑, Ellagic acid supplementation may also improve mood and cognitive function like memory and learning in rats (Gupta et al., 2021).
*memory↑,
*BDNF↑, FA increases catecholamine (dopamine and noradrenaline), brain-derived neurotrophic factor, and ATP levels, and decreases glycogen levels in the limbic system of the mice brain.
*ATP↑,
*Mood↑, antidepressant-like effects of FA observed in this study
*Mood↑, Folate deficiency is associated with depression and dementia
*cognitive↑, Impaired folate metabolism may result in a pattern of cognitive dysfunction that resembles ageing
*other↝, The duration of folate deficiency and of its treatment is as important as the degree of deficiency and the dose of folic acid
*memory↑, 38 folate deficient elderly subjects with depression, lethargy, and memory impairment, folinic acid 50 mg per week for 120 days significantly improved visuomotor performance, visuospatial memory, logical reasoning, associative memory, and activities
*QoL↑,
*homoC↝, confirmed neuropathologically in 76 patients in whom higher plasma homocysteine was associated with a more rapid atrophy of the medial temporal lobes over a three year period
*other↝, impact of folate is slow and cumulative over many months, perhaps because blood-brain barrier mechanisms limit entry to the brain.
*Dose↝, Small doses over the long term may be preferable to larger doses in the short or long term
*BDNF↑, significant increase of BDNF levels in the hippocampus and prefrontal cortex was observed in ethanol-treated mice receiving G115.
*Mood↑, use of G115 as an antidepressant that could be further used as a dietary supplement in comorbid alcohol use and major depressive disorders.
*neuroP↑, neuroprotective effects and their benefits in neuropsychiatric disorders [
*Mood↑, Treatment of the mice with honokiol significantly suppressed the depression-like behavior and increased brain BDNF levels (P < 0.01) in CORT-treated mice.
*BDNF↑,
*BDNF↑, provide novel evidence that luteolin treatment, by restoring microglia alterations and transiently boosting BDNF/TrkB signaling
*Mood↑, Treatment with Luteolin Ameliorates Behavioral Deficits in Cdkl5 +/− Mice
*neuroG↑, Treatment with Luteolin Promotes Neurogenesis in the Hippocampus of Cdkl5 +/− Mice
*TrkB↑, Treatment with Luteolin Transiently Boosts BDNF/TrkB Signaling Pathways in the Cortex of
Cdkl5 +/− Mice
*PSD95↑, upregulating the expression of synaptophysin, postsynaptic density protein 95, brain-derived neurotrophic factor, B cell lymphoma protein-2, superoxide dismutase, and glutathione S-transferase; and decreasing the expression of malondialdehyde, caspa
*BDNF↑,
*SOD↑,
*GSTA1↑,
*MDA↑,
*Casp3↓,
*Mood↑, antidepressant effects of luteolin are mediated by various mechanisms, including anti-oxidative stress, anti-apoptosis, anti-inflammation, anti-endoplasmic reticulum stress, dopamine transport, synaptic protection, hypothalamic–pituitary–adrenal axi
*antiOx↑,
*Apoptosis↓,
*Inflam↓,
*ER Stress↓,
*Aβ↓, Our findings support a beneficial role of total carotenoid consumption, in particular lutein/zeaxanthin, on AD incidence that may be related to the inhibition of brain β-amyloid deposition and fibril formation.
*cognitive↑, lutein-zeaxanthin showed additional inverse associations with AD diagnostic score, neuritic plaque severity, and neurofibrillary tangle density and severity.
*Mood↑, Participants in the lowest quintile of carotenoid intake had higher energy consumption, more depression symptoms, more diabetes and stroke diagnoses, and lower levels of physical activity,
*eff↑, emonstrated statistically significant improvements in skin carotenoid measurements, blood carotenoids, ω-3FAs, and vitamin E concentrations (p < 0.05, for all).
*memory↑, active group also performed better in objective measures of AD severity (i.e., memory and mood), with a statistically significant difference reported in the clinical collateral for memory
*Mood↑,
*QoL↑, Exponential increases in the prevalence of AD and its relentless progressive nature is driving the need for interventions that help to ameliorate symptoms and improve quality of life in AD patients.
*memory↑, Xanthophyll carotenoid concentration increases were significantly greater for Formulation 2 compared to Formulation 1 (p < 0.05), and progression of AD was less for this group (p = 0.003), with carers reporting functional benefits in memory, sight, a
*eff↑, positive outcomes for patients with AD who consumed a combination of xanthophyll carotenoids plus fish oil
*Mood↑,
*neuroP↑, MOO may have a neuroprotective effect in the mouse model of WIRS as evidenced by improving the abnormal behaviors
*Mood↑,
*BDNF↑, through enhancing mRNA expression level of BDNF, inhibited AChE activity, and prevented the increase of MDA level in the brain.
*AChE↓,
*MDA↓,
*antiOx↑, multiple effects such as Moringa oleifera (MO) that have strong anti-oxidative, anti-inflammatory, anticholinesterase, and neuroprotective virtues.
*Inflam↓,
*AChE↓,
*neuroP↑,
*Mood↑, MO improved behavioral deficits such as anxiety-like behavior and hyperactivity and cognitive, learning, and memory impairments.
*cognitive↑,
*memory↑,
*Aβ↓, MO treatment abrogated the Aβ burden to wild-type control mice levels via decreasing BACE1 and AEP and upregulating IDE, NEP, and LRP1 protein levels.
*BACE↓,
*AEP↓,
*IDE↑,
*NEP↑,
*LRP1↑,
*PSD95↑, MO improved synaptic plasticity by improving the decreased GluN2B phosphorylation, the synapse-related proteins PSD95 and synapsin1 levels, the quantity and quality of dendritic spines, and neurodegeneration in the treated mice
*STEP↓, These results suggest that MO modulates the PP2B/DARPP-32/PP1 axis to downregulate STEP activity thereby improving GluN2B Tyr1472 phosphorylation in APP/PS1 mice.
*APP↓, data suggest that MO downregulates the amyloidogenic processing of APP as well as improves Aβ clearance to decrease the Aβ burden in these mice.
*memory↑, Moreover, DMSO exhibited clear influence on the behavior of this mouse line by enhancing hippocampal-dependent spatial memory accuracy, modulating hippocampal-independent olfactory habituation and displaying anxiolytic effect.
*Mood↑, DMSO treatment attenuates anxiety-related behavior
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*memory↑, Nar-treated rats demonstrated improvements in spatial working memory, reduced anxiety-related behaviors, elevated hippocampal CREB and BDNF genes and BDNF protein levels, and reduced AChE activity.
*Mood↑,
*CREB↑,
*BDNF↑,
*AChE↓,
*cognitive↑, These findings suggest that Nar enhances cognitive function and mitigates anxiety
*neuroP↑, exerting neuroprotective effects in the hippocampus.
*Mood↑, piperine has been reported to have antidepressant-like effects in chronically stressed mice
*BDNF↑, Piperettine (2) and piperylin (7) tended to increase endogenous BDNF protein levels.
*memory↑, unlike placebo (PP n = 26), significantly improved memory and prevented “winter blues” in a pre–post comparison
*cognitive↑, PS is efficiently absorbed after oral consumption. A positive influence of PS+PA on memory, mood, and cognition was demonstrated among elderly test subjects.
*Half-Life↝, soy lecithin-derived PS is absorbed and metabolized, with elevated serum levels for at least 1.5 h after an oral dose.
*Mood↑, Nevertheless, a worsening of mood with time was observed within the placebo group, which was not seen in the PS+PA supplementation group
*cognitive↑, clinically significant delay in decline in the Dementia Rating Scale and clock-drawing test as compared to those receiving placebo.
*Mood↑, his formulation holds promise for delaying the decline in cognition, mood, and daily function that accompanies the progression of Alzheimer's disease,
*Mood↑, These observations provide a rational basis for the antidepressant effect of SAM, which has been confirmed in several countries
*BBB↑, SAM either intravenously or orally is associated with a significant rise of CSF SAM, indicating that it crosses the blood-brain barrier in humans.
*Mood↑, review of SAMe in the treatment of major depressive disorder found promising but limited evidence of efficacy and safety to support the use of SAMe as a monotherapy and as an augmentation for other antidepressants.
*BBB↑, SAMe crosses the blood-brain barrier and increases CSF levels
*5HT↑, increases concentrations of CNS monoamine neurotransmitters, serotonin and norepinephrine
*p‑tau↓, SAMe affects site-specific methylation of DNA-promoter regions that regulate gene function, and carboxymethylation of proteins that can regulate b-amyloid and Tau proteins, neuropathological hallmarks of Alzheimer's disease
*Aβ↓,
*other↑, twelve of the nineteen RPCTs showed the antidepressant effect of SAMe to be significantly greater than placebo for depressive syndromes
xCT↓, the inhibition of xCT by SSZ could alleviate depression-like behavior partly via modulating the homeostasis of the glutamate system and dampening neuroinflammation.
Mood↑,
Inflam↓,
glut↓, and the levels of glutamate and pro-inflammatory factors were decreased.
*NRF2↑, Activation of Nrf2 by sulforaphane (SFN) showed fast-acting antidepressant-like effects in mice by activating BDNF as well as by inhibiting the expression of its transcriptional repressors (HDAC2, mSin3A, and MeCP2)
*BDNF↑,
*HDAC2↓,
*Mood↑,
*neuroP↑, Experimental evidence suggests various neuroactive potentials of CP such as memory-enhancing, neuroprotective, and antiepileptic.
*memory↑,
*other↝, analysis predicted a total of five druglike phytochemicals from CP constituents, namely, scopoletin, 4-hydroxycinnamic acid, kaempferol, quercetin, and ayapanin
*AChE↓, scopoletin showed the highest binding affinity with PTGS1, NOS3, PPARG, ACHE, MAOA, MAOB, and TRKB
*MAOA↓,
*MAOB↓,
*TrkB↓,
*tau↓, CP treatment prevented protein and mRNA expressions of tau and amyloid precursor protein (APP) in scopolamine-induced rat brain
*APP↓,
*ROS↓, Scopoletin, a coumarin of CP, attenuated oxidative stress-mediated loss of dopaminergic neurons and increased the efficacy of dopamine in PD model
*Mood↑, In addition, CP improved anxiety, depression, and epileptic seizure
*BDNF↑, improved BDNF expression, 5-HT, DA, NE and antioxidant paradigms in cerebral cortex as well as hippocampus.
*5HT↑,
*antiOx↑,
*IL6↓, silymarin attenuated IL-6, and TNF-α significantly in hippocampus and cerebral cortex in OBX rats.
*TNF-α↓,
*Mood↑, silymarin exhibits anti-depressant-like activity in OBX rats due to alterations in several neurotransmitters, endocrine and immunologic systems, including BDNF, 5-HT, DA, NE, MDA formation, IL-6, and TNF-α in hippocampus
*Aβ↓, Thiamine deficiency exacerbates amyloid beta (Aβ) deposition, tau hyperphosphorylation and oxidative stress.
*p‑tau↓, BFT activates the Nrf2/ARE pathway and is a promising therapeutic agent for the treatment of diseases with tau pathology, such as AD
*ROS↓,
*cognitive↑, Benfotiamine (BFT) rescued cognitive deficits and reduced Aβ burden in amyloid precursor protein (APP)/PS1 mice.
*OS↑, Chronic dietary treatment with BFT increased lifespan, improved behavior, reduced glycated tau, decreased NFTs and prevented death of motor neurons.
*Mood↑,
*neuroP↑,
*Inflam↓, BFT administration significantly ameliorated mitochondrial dysfunction and attenuated oxidative damage and inflammation.
*NRF2↑, BFT and its metabolites (but not thiamine) trigger the expression of Nrf2/antioxidant response element (ARE)-dependent genes in mouse brain
*PGC-1α↑, BFT administration resulted in an upregulation of PGC-1α mRNA levels in P301S TG mice
*AGEs↓, BFT treatment reduced advanced glycation end products
*4-HNE↓, BFT administration led to a significant reduction in the fluorescence signal for both 3-NT and 4-HNE
*NQO1↑, Exposure to BFT upregulated the mRNA levels of NQO1 in TG mice
*COX2↓, Our findings showed that BFT treatment induced a significant decrease in COX-2 (Fig. 7E, P < 0.05), TNF-α (Fig. 7F, P < 0.05), IL-1β (Fig. 7H, P < 0.05), and NF-κB p65
*TNF-α↓,
*IL1β↓,
*NF-kB↓,
*GSK‐3β↓, Exposure to BFT improves cognitive impairment and reduces the amyloid burden in APP/PS1 TG mice in a dose-dependent fashion and was reported to diminish tau phosphorylation, which was attributed to decreased GSK-3β activity (26).
*DNAdam↓, reduces senescence of affected cells, attenuates DNA damage and neuroinflammation in the transgenic APP/PS1 murine model of AD.
*Inflam↓,
*other↓, Elevated cGAS-STING observed in the AD mouse brains and human AD fibroblasts was normalized by NR.
*cognitive↑, This intervention also increased mitophagy with improved cognition and behavior in the APP/PS1 mice
*Mood↑,
*Aβ↓, We have previously shown that pantethine treatment reduces amyloid-β (Aβ)-induced IL-1β release and alleviates pathological metabolic changes in primary astrocyte cultures
*Mood↑, We observed that long-term pantethine treatment significantly reduced glial reactivity and Αβ deposition, and abrogated behavioral alteration in Tg mice.
*neuroP↑, Pantethine elicits broad physiological activities involving multiple cellular pathways. It has been shown to exert neuroprotective effects
*Inflam↓, but also to decrease inflammation and mediate immune responses
*TNF-α↓, We have previously shown that pantethine is able to protect mice against cerebral malaria by preserving blood–brain barrier integrity and by lowering TNF-α levels
*BBB↝, Cysteamine can cross the blood–brain barrier [110] and was shown to induce the release of BDNF (brain-derived neurotrophic factor)
*other↝, The present study demonstrated the efficiency of pantethine to reverse AD features such as astrogliosis, microgliosis, Aβ deposition, and to AD-associated aggressive behavior.
*Dose↝, Based on our results, pantethine, provided routinely as a dietary supplement, could be considered as a serious therapeutic option for preventing, slowing, or halting AD progression.
*Mood↑, Patients with AD have a high prevalence of vitamin D deficiency, which is also associated with low mood and impaired cognitive performance in older people.
*cognitive↑,
*eff↑, Calcitriol, 1αα,25-dihydroxyvitamin D3, is best used for AD because of its active form of vitamin D3 metabolite and its receptor in the central nervous system.
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Risk↓, evidence that vitamin D can reduce the risk of cancer incidence and mortality rates is robust.
angioG↓, Vitamin D reduces angiogenesis around tumors, which is required to deliver nutrients to the tumors
TumMeta↓, and it reduces metastasis into the surrounding stromal tissue, which is generally required for mortality.
AntiCan↑, 9 of the 54 patients in the p53-immunoreactive group treated with vitamin D had a relapse or death during 5 years of follow-up, compared to 14 of 26 in the placebo group
*cognitive↑, Adequate 25(OH)D concentrations are associated with improved cognitive function [105,106] and mood stability [107], particularly in vulnerable populations.
*Mood↑, Vitamin D supplementation has shown promise in enhancing mood and reducing depressive symptoms, with studies indicating improved clinical outcomes in patients receiving vitamin D alongside antidepressants
*BDNF↑, significant positive correlation was found between serum BDNF and zinc levels at baseline.
*Mood↑, Zinc monotherapy improves mood in overweight or obese subjects most likely through increasing BDNF levels.
Showing Research Papers: 1 to 48 of 48
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 48
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
xCT↓, 1,
Core Metabolism/Glycolysis ⓘ
glut↓, 1,
Migration ⓘ
TumMeta↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, Mood↑, 1, Risk↓, 1,
Total Targets: 8
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
4-HNE↓, 1, antiOx↑, 9, GSTA1↑, 1, lipid-P↓, 1, MDA↓, 2, MDA↑, 1, NQO1↑, 1, NRF2↑, 2, ROS↓, 6, SOD↑, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, PGC-1α↑, 1,
Core Metabolism/Glycolysis ⓘ
CREB↑, 4, glucose↓, 1, homoC↝, 1,
Cell Death ⓘ
Apoptosis↓, 2, Casp3↓, 1,
Transcription & Epigenetics ⓘ
Ach?, 1, other?, 1, other↓, 7, other↑, 3, other↝, 4,
Protein Folding & ER Stress ⓘ
ER Stress↓, 1,
DNA Damage & Repair ⓘ
DNAdam↓, 1,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 1, HDAC2↓, 1, neuroG↑, 1,
Migration ⓘ
APP↓, 2, LRP1↑, 1,
Barriers & Transport ⓘ
BBB↑, 5, BBB↝, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 10, Inflam↑, 1, NF-kB↓, 1, TNF-α↓, 4,
Synaptic & Neurotransmission ⓘ
5HT↓, 1, 5HT↑, 6, AChE↓, 6, AChE∅, 1, BChE↓, 2, BDNF↑, 18, GABA↑, 2, MAOA↓, 1, PSD95↑, 2, tau↓, 1, p‑tau↓, 2, TrkB↓, 1, TrkB↑, 3,
Protein Aggregation ⓘ
AEP↓, 1, AGEs↓, 1, Aβ↓, 5, BACE↓, 2, IDE↑, 1, MAOB↓, 1, NEP↑, 1,
Drug Metabolism & Resistance ⓘ
Dose↝, 2, eff↑, 6, eff↝, 1, Half-Life↝, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, cognitive↑, 19, hepatoP↑, 1, memory↑, 17, Mood↑, 48, motorD↑, 2, neuroP↑, 10, OS↑, 1, QoL↑, 4, Risk↓, 1, Sleep↑, 2, STEP↓, 1,
Total Targets: 75
Scientific Paper Hit Count for: Mood, Behaviour
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include :
-low or high Dose
-format for product, such as nano of lipid formations
-different cell line effects
-synergies with other products
-if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:% prod#:% Target#:1362 State#:% Dir#:2
wNotes=on sortOrder:rid,rpid
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