Extra virgin olive oil found to prevent Alzheimer’s and protect the brain’s memory function

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Natural News

When people talk about the health benefits of extra-virgin olive oil, it is usually linked to heart health. However, its effects on a different organ have been in the news lately: The brain. 

Researchers from Temple University have discovered that extra-virgin olive oil (EVOO) can not only help protect against memory loss, but it can also alleviate the conditions associated with Alzheimer’s disease. They reached their conclusion following studies involving mice with induced dementia.

The mice were divided into two groups, one of which was given a diet that was enriched with extra-virgin olive oil. The oil was introduced when the mice were just six months old and had not yet begun to display symptoms of Alzheimer’s.

While the two groups of mice did not show any differences in their appearance immediately following their respective diets, the neuron connections in the brains of the mice on the EVOO diet were better preserved at nine and 12 months, and they also showed better learning and memory ability on tests.

Alzheimer’s disease is believed to begin with a reduction in the brain’s autophagy process, which entails the removal of the toxins and intracellular debris that are firm markers of the illness. Olive oil is able to activate this important process and reduce brain inflammation, thereby protecting against Alzheimer’s.

The consumption of olive oil also helps to reduce the formation of harmful brain structures, such as neurofibrillary tangles and amyloid-beta plaques. Previous research has linked the presence of such structures to an individual’s likelihood of developing Alzheimer’s, with neurofibrillary tangles believed to contribute to the poor memory that is often seen in Alzheimer’s patients.

Senior researcher Professor Domenico Pratico of the Lewis Klein School of Medicine remarked: “Thanks to the autophagy activation, memory and synaptic integrity were preserved, and the pathological effects in animals otherwise destined to develop Alzheimer’s disease were significantly reduced.”

Next, the researchers would like to determine if introducing olive oil at a more advanced age can reverse or stop the illness. This is crucial because many people don’t start to suspect dementia until the illness is already present.

With five million Americans currently living with Alzheimer’s and as many as 16 million expected to develop it by 2050, the time to find a solution is now. Dementia is already a leading cause of poor health and disability, and it’s the sixth-leading cause of death in our nation. In addition to its effects on the patients, this heartbreaking illness also places a tremendous burden on family members and caregivers.

Olive oil’s benefits extend beyond preventing dementia

Avoiding dementia is not the only reason to add more olive oil to your diet. A recent study from Copenhagen University Hospital involving 182 men aged 20 to 60 found that those who consumed a quarter cup of olive oil per day had an average reduction in oxidative damage to DNA cells of 13 percent. It has also been linked to a reduction in stroke and heart disease risk, protection against depression, and healthy cholesterol levels.

However, when you’re looking to increase your intake of olive oil, make sure you know what you’re getting as fraud is widespread in the industry. Many of our country’s best-selling brands failed to meet IOC standards in tests due to adulteration, oxidation, or poor quality. Italian extra-virgin olive oil is commonly mixed with inferior olive oils that are cheaper to produce, or even other types of oil entirely. Experts say that real olive oil starts to solidify when refrigerated.

With so many great health benefits and new ones constantly being discovered by researchers, there is no reason not to start consuming more of this healthy oil.

Sources:

USAToday.com

DailyMail.co.uk

ALZ.org

NaturalNews.com

NaturalNews.com

Single brain trauma affects an enzyme associated with Alzheimer's disease

Caregivers, and healthcare professionals, here is some great information

Here is a great dementia resource for caregivers and healthcare professinals,

Your residents will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Tufts Now

By 

News Staff

A study, performed in mice and utilizing post-mortem samples of brains from patients with Alzheimer’s disease, found that a single event of a moderate-to-severe traumatic brain injury (TBI) can disrupt proteins that regulate an enzyme associated with Alzheimer’s. The paper, published in the Journal of Neuroscience, identifies the complex mechanisms that result in a rapid and robust post-injury elevation of the enzyme BACE1 in the brain. These results may lead to the development of a drug treatment that targets this mechanism to slow the progression of Alzheimer’s disease.

“A moderate-to-severe TBI, or head trauma, is one of the strongest environmental risk factors for Alzheimer’s disease. A serious TBI can lead to a dysfunction in the regulation of the enzyme BACE1. Elevations of this enzyme cause elevated levels of amyloid-beta, the key component of brain plaques associated with senility and Alzheimer’s disease,” says first author Kendall Walker, postdoctoral associate in the department of neuroscience at Tufts University School of Medicine (TUSM). 

Moderate-to-severe TBIs are caused most often by traumas such as severe falls or motor vehicle accidents that result in a loss of consciousness. Not all traumas to the head result in a TBI. According to the Centers for Disease Control and Prevention, each year 1.7 million people sustain a TBI. Concussions, the mildest form of a TBI, account for about 75 percent of all TBIs. Studies have linked repeated head trauma to brain disease, and some previous studies have linked single events of brain trauma to brain disease, such as Alzheimer’s. Alzheimer’s disease currently affects as many as 5.1 million Americans and is the most common cause of dementia in adults age 65 and over.

Building on her previous work, Giuseppina Tesco, an assistant professor of neuroscience in the School of Medicine, led a research team that first used an in vivo model to determine how a single episode of TBI could alter the brain. In the acute phase (first two days) following injury, levels of two intracellular trafficking proteins (GGA1 and GGA3) were reduced, and an elevation of BACE1 enzyme level was observed.

Next, in an analysis of post-mortem brain samples from patients with Alzheimer’s disease, the researchers found that GGA1 and GGA3 levels were reduced while BACE1 levels were elevated in the brains of Alzheimer’s disease patients compared to the brains of people without Alzheimer’s disease, suggesting a possible inverse association.

In an additional experiment using a mouse strain genetically modified to express the reduced level of GGA3 that was observed in the brains of Alzheimer’s disease patients, the team found that one week following traumatic brain injury, BACE1 and amyloid-beta levels remained elevated even when GGA1 levels had returned to normal. The research suggests that reduced levels of GGA3 were solely responsible for the increase in BACE 1 levels and therefore the sustained amyloid-beta production observed in the sub-acute phase, or seven days, after injury.

“When the proteins are at normal levels, they work as a clean-up crew for the brain by regulating the removal of BACE1 enzymes and facilitating their transport to lysosomes within brain cells, an area of the cell that breaks down and removes excess cellular material. BACE1 enzyme levels may be stabilized when levels of the two proteins are low, likely caused by an interruption in the natural disposal process of the enzyme,” said Tesco, who is also member of the neuroscience program faculty at the Sackler School of Graduate Biomedical Sciences at Tufts.

“We found that GGA1 and GGA3 act synergistically to regulate BACE1 post-injury. The identification of this interaction may provide a drug target to therapeutically regulate the BACE1 enzyme and reduce the deposition of amyloid-beta in Alzheimer’s patients,” she continued. “Our next steps are to confirm these findings in post-mortem brain samples from patients with moderate-to-severe traumatic brain injuries.”

Expand+Midlife psychological stress and risk of dementia: a 35-year longitudinal population study

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Brain

Lena Johansson1, Xinxin Guo1, Margda Waern1, Svante Östling1, Deborah Gustafson1,2, Calle Bengtsson3 and Ingmar Skoog1
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The number of people with dementia has increased dramatically with global ageing. Nevertheless, the pathogeneses of these diseases are not sufficiently understood. The present study aims to analyse the relationship between psychological stress in midlife and the development of dementia in late-life. A representative sample of females (n = 1462) aged 38–60 years were examined in 1968–69 and re-examined in 1974–75, 1980–81, 1992–93 and 2000–03. Psychological stress was rated according to a standardized question in 1968, 1974 and 1980. Dementia was diagnosed according to Diagnostic and Statistical Manual of Mental Disorders criteria based on information from neuropsychiatric examinations, informant interviews, hospital records and registry data. During the 35-year follow-up, 161 females developed dementia (105 Alzheimer’s disease, 40 vascular dementia and 16 other dementias). We found that the risk of dementia (hazard ratios, 95% confidence intervals) was increased in females reporting frequent/constant stress in 1968 (1.60, 1.10–2.34), in 1974 (1.65, 1.12–2.41) and in 1980 (1.60, 1.01–2.52). Frequent/constant stress reported in 1968 and 1974 was associated with Alzheimer’s disease. Reporting stress at one, two or three examinations was related to a sequentially higher dementia risk. Compared to females reporting no stress, hazard ratios (95% confidence intervals) for incident dementia were 1.10 (0.71–1.71) for females reporting frequent/constant stress at one examination, 1.73 (1.01–2.95) for those reporting stress at two examinations and 2.51 (1.33–4.77) at three examinations. To conclude, we found an association between psychological stress in middle-aged women and development of dementia, especially Alzheimer’s disease. More studies are needed to confirm our findings and to study potential neurobiological mechanisms of these associations.