Components that help in cerebroprotective action are substances that can contribute to protecting and improving brain health. Here are some examples:

• Omega-3 Fatty Acids. Found in fatty fish, flaxseeds, and walnuts, they support neuronal and cognitive health.
• Antioxidants. Such as vitamin C, vitamin E, and flavonoids, protect brain cells from free radical damage (1).
• Curcumin. The active ingredient in turmeric, known for its neuroprotective properties (2).
• Alpha-Lipoic Acid. An antioxidant that can help protect brain cells.
• Resveratrol. Found in grapes and red wine, has beneficial effects on brain health (3).
• Bacopa Monnieri. A plant traditionally used to improve memory and cognitive function.
• Lecithin. Rich in choline, important for the health of brain cell membranes.
• Green Tea. Contains L-theanine and antioxidants that can benefit brain health.
• Regular Physical Exercise. Improves blood circulation and overall brain health.

Components that can contribute to or exacerbate regular brain function include various factors that can negatively affect brain health. Here are some examples

• Alcohol. Excessive consumption can damage brain cells and alter brain function.
• Refined Sugars. High intake can lead to blood sugar fluctuations, negatively affecting brain function.

• Trans and Saturated Fats. Found in fried and processed foods, can contribute to brain inflammation.
• Nicotine. Can cause addiction and alter neurochemical processes in the brain.
• Excessive Caffeine. High consumption can disturb sleep and neurochemical balance.
• Lack of Sleep. Sleep deprivation can impair cognitive function and memory.
• Chronic Stress. Can damage brain cells and reduce neuroplasticity.
• Environmental Pollutants. Exposure to toxic substances can have negative effects on the brain.
• Deficiency in Essential Nutrients. Such as omega-3, vitamins, and minerals, can negatively affect brain health.
• Sedentary Lifestyle. Lack of physical exercise can reduce blood flow to the brain and its functionality.

The reports  provided on Tiiips website are for informational purposes only and should not replace medical advice. Always consult a healthcare professional before making health-related decisions.

References_____________________________________________________________________

(1) Bora, K. S., & Sharma, A. (2011). Evaluation of antioxidant and cerebroprotective effect of Medicago sativa Linn. against ischemia and reperfusion insult. Evidence-based complementary and alternative medicine, 2011.

Abstract. Antioxidants have been the focus of studies for developing neuroprotective agents to be used in the therapy for stroke, which is an acute and progressive neurodegenerative disorder. Medicago sativa (MS) has a long tradition of use as ayurvedic and homoeopathic medicine in central nervous system disorders. The plant has been reported to have antioxidant, anti-inflammatory and antidiabetic effects. Therefore, the present study was designed to investigate the neuroprotective effect of methanol extract of MS on ischemia and reperfusion-induced cerebral injury in mice. Bilateral carotid artery occlusion (BCAO) for 15 min followed by 24-h reperfusion, resulted in significant elevation in infarct size, xanthine oxidase (XO) activity, superoxide anion (O•−2) production and thiobarbituric acid-reactive substance (TBARS) levels, and significant depletion in endogenous antioxidant [reduced glutathione (GSH), superoxide dismutase (SOD) and total tissue sulfhydryl (T-SH) groups] systems in mice brain. Further, BCAO led to impairment in short-term memory and motor coordination. Pre-treatment with MS (100 or 200 mg kg−1, p.o.) markedly reduced cerebral infarct size, XO, O•−2 and TBARS levels, significantly restored GSH, SOD and T-SH levels and attenuated impairment in short-term memory and motor coordination. In addition, MS directly scavenged free radicals generated against a stable radical 1,1-diphenyl-2-picrylhydrazyl and O•−2 generated in phenazine methosulphate-nicotinamide adenine dinucleotide systems, and also inhibited XD/XO conversion and resultant O•−2 production. The data from this study suggest that treatment with MS enhances the antioxidant defense against BCAO-induced global cerebral ischemia and exhibits neuroprotective activity.

(2) Dong, W., Yang, B., Wang, L., Li, B., Guo, X., Zhang, M., ... & Zhao, R. (2018). Curcumin plays neuroprotective roles against traumatic brain injury partly via Nrf2 signaling. Toxicology and applied pharmacology, 346, 28-36.

Abstract. Traumatic brain injury (TBI), which leads to high mortality and morbidity, is a prominent public health problem worldwide with no effective treatment. Curcumin has been shown to be beneficial for neuroprotection in vivo and in vitro, but the underlying mechanism remains unclear. This study determined whether the neuroprotective role of curcumin in mouse TBI is dependent on the NF-E2-related factor (Nrf2) pathway. The Feeney weight-drop contusion model was used to mimic TBI. Curcumin was administered intraperitoneally 15 min after TBI induction, and brains were collected at 24 h after TBI. The levels of Nrf2 and its downstream genes (Hmox-1, Nqo1, Gclm, and Gclc) were detected by Western blot and qRT-PCR at 24 h after TBI. In addition, edema, oxidative damage, cell apoptosis and inflammatory reactions were evaluated in wild type (WT) and Nrf2-knockout (Nrf2-KO) mice to explore the role of Nrf2 signaling after curcumin treatment. In wild type mice, curcumin treatment resulted in reduced ipsilateral cortex injury, neutrophil infiltration, and microglia activation, improving neuron survival against TBI-induced apoptosis and degeneration. These effects were accompanied by increased expression and nuclear translocation of Nrf2, and enhanced expression of antioxidant enzymes. However, Nrf2 deletion attenuated the neuroprotective effects of curcumin in Nrf2-KO mice after TBI. These findings demonstrated that curcumin effects on TBI are associated with the activation the Nrf2 pathway, providing novel insights into the neuroprotective role of Nrf2 and the potential therapeutic use of curcumin for TBI.

(3) Orsu, P., Murthy, B. V. S. N., & Akula, A. (2013). Cerebroprotective potential of resveratrol through anti-oxidant and anti-inflammatory mechanisms in rats. Journal of Neural Transmission, 120, 1217-1223.

Abstract. Oxidative stress and inflammation are two important pathological mechanisms involved in cerebral ischemia and reperfusion injury. In pathological conditions such as cerebral infarction, the free radical production is greater than that of elimination by endogenous anti-oxidant system, by this undesirable effect brain is highly injured. Resveratrol is reported to have anti-oxidant and anti-inflammatory, athero-protective activities. Therefore, the aim of the present study is to evaluate the therapeutic potential of resveratrol against cerebral infarction induced by ischemia and reperfusion injury in Wistar rats. Bi-common carotid occlusion followed by 4 h reperfusion model was used to induce cerebral infarction. Percent infarction, oxidative stress markers (malondialdehyde, catalase, superoxide dismutase) and inflammatory markers (myeloperoxidase, TNF-α, IL-6, ICAM-1 and IL-10) were measured. TNF-α, IL-6, IL-10, and intracellular adhesive molecule-I (ICAM-1) levels were quantified by enzyme-linked immunosorbent assay (ELISA). Resveratrol produced significant dose-dependent reduction in percent cerebral infarct volume. At resveratrol 20 mg/kg dose, there was a significant reduction in oxidative stress and inflammatory markers like malondialdehyde, TNF-α, IL-6, myeloperoxidase and ICAM-I and in contrast there was a significant increase in anti-oxidants and anti-inflammatory markers like superoxide dismutase, catalase and IL-10 levels. Resveratrol showed significant cerebroprotective action mediated by anti-oxidant and anti-inflammatory mechanisms.