neuroprotective effects Archives - Amazing Health Advances

Exciting Potential: How to IMPROVE Your Brain Function with Melatonin

AHA Publisher — Mon, 06 Dec 2021 08:00:01 +0000

Lori Alton via Naturalhealth365 – According to a recent report published in Alzheimer’s and Dementia Journal, Alzheimer’s disease – the sixth leading cause of death in the United States – claimed over 121,000 lives in 2019 alone, before the pandemic had swept the nation. Alzheimer’s disease claimed over 121,000 lives in 2019 alone, before the pandemic had swept the nation Meanwhile, the Alzheimer’s Association has released a sobering new statistic – deaths from Alzheimer’s disease and other forms of dementia have increased by a significant 16 percent since the onset of COVID-19. However, a natural intervention for the condition is casting a ray of hope. In a recent review article in the peer-reviewed journal Revue Neurologique, researchers report that the natural hormone melatonin shows exciting potential to prevent and even alleviate neurodegenerative diseases, such as Alzheimer’s and Parkinson’s disease. In fact, the impressed scientists even concluded that “melatonin may be the solution we have been looking for.” Why are they so hopeful about the neuroprotective effects of melatonin? Let’s find out. Melatonin Sharpens Memory and Increases Formation of New Brain Cells Melatonin, commonly known as the “sleep hormone,” is produced in the pineal gland in the brain. This critical hormone regulates the circadian rhythms and the sleep-wake cycle while improving the overall quality of sleep. Researchers have long believed that melatonin may improve memory and cognition. And, the “proof is in the pudding.” In an older – but still influential – placebo-controlled study published in Psychopharmacology, 50 young men were given a one-time, 3-mg dose of melatonin. The effects were rapid, unequivocal, and clear-cut, with participants in the melatonin group able to recall more objects from a memorized list than those in the placebo group! The researchers concluded that melatonin could suppress the stress-induced hormones that affect memory processing. But does melatonin work for older individuals? Neuroprotective Effects of Melatonin May Improve Alzheimer’s Disease While melatonin exists in generous amounts in young people, it appears that supplies decrease with age. The review authors noted that patients with Alzheimer’s disease have lower melatonin levels than healthy people of the same age – and that melatonin deficiency may play a vital role in the development of Alzheimer’s disease and dementia. Raising melatonin levels in the body may not only combat age-related memory decline and cognitive impairment – but, the neuroprotective effects of melatonin may help slow the progression of neurodegenerative diseases. Scientists point out that almost half of all Alzheimer’s patients have problems with sleep. Lack of sleep is associated with increased plaque deposits of beta-amyloid, a protein strongly implicated in the development of the disease. Melatonin promotes the type of refreshing sleep needed for efficient brain function and accurate memory, with clinical studies supporting the ability of the hormone to slow the progression of cognitive disorders. Melatonin Improves Brain Function Through Multiple Mechanisms The neuroprotective effects of melatonin can be attributed to many factors. Melatonin appears to cushion the brain from the effects of “stress” hormones – such as epinephrine, cortisol, and norepinephrine – which can impair memory. It also increases levels of a protein known as a brain-derived neurotrophic factor (BDNF), which increases the formation of neurons. In addition, cell studies have shown that melatonin improves plasticity, the ability of the brain to change and adapt to new experiences. Finally, melatonin is a potent antioxidant that scavenges harmful free radicals (reactive oxygen species) that would otherwise cause oxidative stress and damage to cells and tissues, thereby triggering disease. Impressively, studies have shown that melatonin can even help to counter damage from memory-impairing drugs, including the chemotherapy drug fluorouracil and the anti-nausea medication scopolamine. Researchers theorize that melatonin achieved this by promoting cell division in the hippocampus, the brain’s “memory center.” Improve Sleep and Cognition with Melatonin Natural health experts advise using a high-quality melatonin formulation from a reputable vendor, with typical amounts ranging between 0.5 mg and 10 mg a day. To promote restful sleep, melatonin should be taken about 30 minutes before bedtime. However, if you take melatonin to correct out-of-sync circadian rhythms over the long term, it should be taken two to three hours before bedtime. Naturally, check with your integrative doctor before supplementing with melatonin. As a “pro” tip: The amino acid tryptophan is needed for the body to produce melatonin. You can raise your dietary intake of tryptophan with raw cheese, pasture-raised organic chicken, pumpkin seeds, and wild caught fish. In addition to the devastating human toll of Alzheimer’s disease – such as loss of precious memories and the ability to function independently – the financial burden of this illness is staggering. In fact, the national cost for Alzheimer’s and other dementias in 2021 is expected to clock in at $355 billion. No doubt, the relatively inexpensive, non-toxic, convenient, and safe choice of consuming melatonin may well emerge as an effective natural intervention for this cruel health issue. Sources for this article include: Alzheimers.org NIH.gov Healthline.com NIH.gov To read the original article click here.

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Component Derived from Turmeric Essential Oil Exhibits Neuroprotective Effects

AHA Publisher — Fri, 23 Jul 2021 07:00:47 +0000

Kumamoto University via News-Medical – Researchers from Kumamoto University, Japan have found that a component derived from turmeric essential oil, aromatic turmerone (ar-turmerone), and its derivatives act directly on dopaminergic nerves to create a neuroprotective effect on tissue cultures of a Parkinson’s disease model. This appears to be due to enhanced cellular antioxidant potency from the activation of Nrf2. The researchers believe that the ar-turmerone derivatives identified in this study can be used as new therapeutic agents for Parkinson’s disease. Parkinson’s disease is a neurodegenerative disease caused by the selective death of dopaminergic neurons that transmit information from the substantia nigra of the midbrain to the striatum which results in decreased dopamine production. Symptoms include limb tremors, immobility, muscle rigidity, and other movement disorders. Treatments, such as dopamine supplements, are currently available but there still no way to inhibit dopaminergic neurodegeneration. Previous studies have reported that the inflammatory response caused by the activation of microglia (cells responsible for immune function in the brain) is observed in the substantia nigra of the midbrain of Parkinson’s disease patients. Further experiments designed to mimic the in vivo state of the midbrain (midbrain slice culture) revealed that microglial activation triggers the selective degeneration of dopaminergic neurons in the substantia nigra, and that nitric oxide (NO) derived from activated microglia was involved in the neurodegeneration. These findings suggest that compounds with anti-inflammatory effects on microglia may suppress dopaminergic degeneration. Thus, researchers analyzed aromatic tumerone (ar-turmerone), a major component of turmeric essential oil that has been reported to exhibit anti-tumor and anti-inflammatory effects on microglia. They used the BV2 microglial cell line and midbrain slice cultures to 1) determine if ar-turmerone suppresses dopaminergic neurodegeneration through its anti-inflammatory effects, and 2) identify structurally similar compounds (derivatives) that might have stronger anti-inflammatory and neuroprotective effects. Ar-turmerone has an asymmetric carbon (S-Tur) so researchers prepared eight analogues and attempted to identify those with stronger anti-inflammatory effects. They used the inhibitory effects on the inflammatory response as induced by lipopolysaccharide (LPS)-stimulated activation of BV2 cells as an indicator. The analogues with stronger anti-inflammatory effects than S-Tur were (R)-ar-turmerone (R-Tur), ar-atlantone (Atl), and analog 2 (A2). To examine whether these compounds, including S-Tur, have an inhibitory effect on dopaminergic degeneration, researchers then observed midbrain slice cultures in which microglial activation was induced by interferon-γ and LPS stimulation (IFN-γ/LPS). All four compounds significantly suppressed a decrease in the number of dopaminergic neurons as induced by IFN-γ/LPS. However, the production of NO, which is released from activated microglia and is involved in dopaminergic neurodegeneration, was not inhibited at all. In addition, three compounds, S-Tur, Atl and A2, inhibited dopaminergic degeneration that is induced by MPP+, a toxin that selectively damages dopaminergic neurons independent of microglial activity. These results indicate that S-Tur and its derivatives, Atl and A2, have a direct effect on dopaminergic neurons and exhibit neuroprotective effects. Furthermore, analysis using dopaminergic progenitor cell lines and midbrain slice cultures revealed that the neuroprotective effects of Atl and A2 are mediated by activation of Nrf2, a transcription factor that enhances the antioxidant potency of cells. “Our study elucidated a new mechanism by which ar-turmerone and its derivatives directly protect mesencephalic slice dopaminergic neurons, independent of their previously reported anti-inflammatory effects on microglia. We showed that two derivatives, Atl and A2, exhibit neuroprotective effects by increasing the expression of antioxidant proteins through the activation of Nrf2. In particular, the analog A2 identified in this study is a potent activator of Nrf2 and is assumed to have a strong antioxidant effect. We think it is possible that this compound may be a new dopaminergic neuroprotective agent for Parkinson’s disease treatment, and it could also be used to treat other diseases caused by oxidative stress, such as liver and kidney diseases.” (Takahiro Seki, Associate Professor, Kumamoto University) This research was posted online in Cells on 3 May 2021. To read the original article click here.

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