A Surprising Way to Tell If You’ll Develop Alzheimer’s

Live in the Now

The statistics on Alzheimer’s disease are overwhelming. More than 5 million Americans are living with Alzheimer’s disease. One in eight older Americans has the condition, and Alzheimer’s is the sixth leading cause of death in the United States.

But there is another little-known stat that is equally, if not more, startling. Among cognitively normal people over the age of 75, about one-third has sufficient amyloid plaques and neurofibrillary tangles to meet the criteria for Alzheimer’s disease.

These plaques and tangles are especially prominent in those who have Alzheimer’s and contribute to the degradation of neurons in the brain. But they also develop in many elderly people, even those who do not have Alzheimer’s.

It’s these cases — referred to as asymptomatic Alzheimer’s disease (ASYMAD) — that researchers find particularly fascinating. People with ASYMAD have all the physical characteristics that could lead to the progression of Alzheimer’s disease, but have managed to avoid it. If researchers figure out how, then that could lead the way to better, more effective prevention and treatment measures for Alzheimer’s, which are both sorely lacking right now.

Negativity Hurts the Brain

A team of researchers recently hypothesized that certain personality traits contribute to the cognitive resilience of ASYMAD. They compared the personality traits of those who subsequently developed clinical dementia with those who subsequently died cognitively normal, but with plaques and tangles indicative of Alzheimer’s discovered at autopsy.

And the results of this study may just want to make you turn that frown upside down, especially if you want to protect your brain.

The subjects in this study were also participants in the Baltimore Longitudinal Study of Aging, a study of physical and psychological aging. All agreed to have an autopsy of the brain following their death.

Researchers analyzed data obtained from 111 of the participants who completed personality tests at least once before the onset of cognitive decline, and who underwent autopsies after death.

Personality traits were measured using a 240-item questionnaire that looked at 30 facets of personality, six for each of the five major dimensions of personality: neuroticism, extraversion, openness, conscientiousness and agreeableness.

As for neuropathology, participants were divided into three groups based on their cognitive health in their last year of life and their autopsy results:

1. Normal: Patients had no history of cognitive decline and autopsies showed no amyloid beta plaques or other signs of Alzheimer’s.

2. ASYMAD: Patients had no history of cognitive decline, but the autopsies showed amyloid beta plaques in the brain.

3. AD: Patients received clinical diagnosis of dementia and/or Alzheimer’s disease while alive, and autopsies revealed amyloid beta plaques and other signs indicative of Alzheimer’s.

Looking at the results of the autopsies and the personality questionnaires, researchers discovered that those who had greater emotional resilience and conscientiousness had lower risk of developing dementia, even if their autopsies revealed plaques or other signs of Alzheimer’s.

More specifically, ASYMAD patients scored lower on their personality questionnaires on negative traits like neuroticism, vulnerability to stress, anxiety and depression, compared with controls and to those who actually developed Alzheimer’s disease.

In addition, low scores on conscientiousness were strongly associated with the development of clinical dementia.

Researchers believe those who are more emotionally stable and conscientious may have greater resilience because they are generally healthier and engage in behaviors that reduce the risk of dementia — like exercising and abstaining from tobacco use. In addition, emotionally stable people tend to have better metabolic and inflammatory risk profiles and are less likely to have depression — all of which have been linked to dementia.

Also, they found that personality might be related to the severity of disease. Specifically, high neuroticism and low agreeableness were linked to more advanced spread of tangles. And skepticism, cynicism and being manipulative/deceptive were the characteristics associated with the most severe amyloid plaques and tangles.

This new knowledge of how personality traits affect the development of dementia allows us to see just how much of a role attitude plays in our overall health.

The more negative your overall demeanor, the more it will affect your health, possibly leading to cognitive decline and Alzheimer’s disease. Conversely, even if you are at physically high risk of Alzheimer’s, having a positive attitude toward life could delay or stop the progression of the disease. All the more reason to spend as much time as you can smiling, laughing and appreciating all the little things in your life.

Marijuana Compound Found Superior To Drugs For Alzheimer’s

GreenMedInfo
by Sayer Ji

Could the active ingredient in marijuana, responsible for its characteristic “high,” help turn the tide against the accelerating Alzheimer’s epidemic?

A remarkable study published in the journal Molecular Pharmacology in 2006, found that this long vilified plant contains a compound with not one, but two therapeutic properties ideal for addressing both the surface symptom (memory problems) and root cause (brain plaque) of Alzheimer’s disease.[i] This is an ironic finding, considering that the prevailing stereotype is that using marijuana “fries” the brain, leading to debilitating memory issues.

Researchers discovered that the psychoactive component of marijuana, Δ9-tetrahydrocannabinol (THC), both “competitively inhibits the enzyme acetylcholinesterase (AChE) as well as prevents AChE-induced amyloid β-peptide (Aβ) aggregation.”

On the first account, THC’s ability to inhibit the AChE enzyme, is not unlike the mechanism of action behind most Alzheimer’s drugs on the market today. Drugs like donepezil (trade name Aricept), for instance, by targeting and inhibiting the brain enzyme acetylcholinesterase (AChE), result in an increase in brain levels of this neurotransmitter, which in turn, results in symptom reduction, i.e. improved memory. Donepezil, however, is riddled with controversy due its well-known association with seizures, which likely reflects its intrinsic neurotoxicity. It is, in fact, a chemical in the same general chemical class as venom, insecticides and chemical war agents, such as nerve gas.

On the second account, THC’s ability to prevent the acetylcholinesterase-associated amyloid β-peptide (Aβ) aggregation, i.e. brain plaque, indicates that it may, as the researchers noted, “directly impact Alzheimer’s disease pathology.” In fact, they found “Compared to currently approved drugs prescribed for the treatment of Alzheimer’s disease, THC is a considerably superior inhibitor of Aβ aggregation, and this study provides a previously unrecognized molecular mechanism through which cannabinoid molecules may directly impact the progression of this debilitating disease.”

What is so encouraging about this research, and which the researchers described as “noteworthy,” is the following:

THC is a considerably more effective inhibitor of AChE-induced Aβ deposition than the approved drugs for Alzheimer’s disease treatment, donepezil and tacrine, which reduced Aβ aggregation by only 22% and 7%, respectively, at twice the concentration used in our studies.7 Therefore, AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer’s disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing Aβ aggregation, thereby simultaneously treating both the symptoms and progression of Alzheimer’s disease.

THC, of course, is only one of a wide range of cannabinoids in the plant marijuana. Not only is there already plentiful information on the neuroprotective properties of marijuana compounds, but there is also a sizeable body of clinical and/or biomedical research indicating the medicinal value of this plant in over 150 health conditions. To view this research visit our Medical Marijuana Research page.

Alzheimer’s could be the most catastrophic impact of junk food

The Guardian
by George Monbiot

When you raise the subject of over-eating and obesity, you often see people at their worst. The comment threads discussing these issues reveal a legion of bullies who appear to delight in other people’s problems.

When alcoholism and drug addiction are discussed, the tone tends to be sympathetic. When obesity is discussed, the conversation is dominated by mockery and blame, though the evidence suggests that it may be driven by similar forms of addiction.

I suspect that much of this mockery is a coded form of snobbery: the strong association between poor diets and poverty allows people to use this issue as a cipher for something else they want to say, which is less socially acceptable.

But this problem belongs to all of us. Even if you can detach yourself from the suffering caused by diseases arising from bad diets, you will carry the cost, as a growing proportion of the health budget will be used to address them. The cost – measured in both human suffering and money – could be far greater than we imagined. A large body of evidence now suggests that Alzheimer’s is primarily a metabolic disease. Some scientists have gone so far as to rename it: they call it type 3 diabetes.

New Scientist carried this story on its cover on 1 September; since then I’ve been sitting in the library, trying to discover whether it stands up. I’ve now read dozens of papers on the subject, testing my cognitive powers to the limit as I’ve tried to get to grips with brain chemistry. Though the story is by no means complete, the evidence so far is compelling.

About 35 million people suffer from Alzheimer’s disease worldwide; current projections, based on the rate at which the population ages, suggest that this will rise to 100 million by 2050. But if, as many scientists now believe, it is caused largely by the brain’s impaired response to insulin, the numbers could rise much further. In the United States, the percentage of the population with type 2 diabetes, which is strongly linked to obesity, has almost trebled in 30 years. If Alzheimer’s, or “type 3 diabetes”, goes the same way, the potential for human suffering is incalculable.

Insulin is the hormone that prompts the liver, muscles and fat to absorb sugar from the blood. Type 2 diabetes is caused by excessive blood glucose, resulting either from a deficiency of insulin produced by the pancreas, or resistance to its signals by the organs that would usually take up the glucose.

The association between Alzheimer’s and type 2 diabetes is long-established: type 2 sufferers are two to three times more likely to be struck by this form of dementia than the general population. There are also associations between Alzheimer’s and obesity and Alzheimer’s and metabolic syndrome (a complex of diet-related pathologies).

Researchers first proposed that Alzheimer’s was another form of diabetes in 2005. The authors of the original paper investigated the brains of 54 corpses, 28 of which belonged to people who had died of the disease. They found that the levels of both insulin and insulin-like growth factors in the brains of Alzheimer’s patients were much lower than those in the brains of people who had died of other causes. Levels were lowest in the parts of the brain most affected by the disease.

Their work led them to conclude that insulin and insulin-like growth factor are produced not only in the pancreas but also in the brain. Insulin in the brain has a host of functions: as well as glucose metabolism, it helps to regulate the transmission of signals from one nerve cell to another, and affects their growth, plasticity and survival.

Experiments conducted since then seem to support the link between diet and dementia, and researchers have begun to propose potential mechanisms. In common with all brain chemistry, these tend to be fantastically complex, involving, among other impacts, inflammation, stress caused by oxidation, the accumulation of one kind of brain protein and the transformation of another. I would need the next six pages of this paper even to begin to explain them, and would doubtless get it wrong (if you’re interested, please follow the links on my website).

Plenty of research still needs to be done. But, if the current indications are correct, Alzheimer’s disease could be another catastrophic impact of the junk food industry, and the worst discovered so far. Our governments, as they are in the face of all our major crises, seem to be incapable of responding.

In this country, as in many others, the government’s answer to the multiple disasters caused by the consumption of too much sugar and fat is to call on both companies and consumers to regulate themselves. Before he was replaced by someone even worse, the former health secretary, Andrew Lansley, handed much of the responsibility for improving the nation’s diet to food and drink companies – a strategy that would work only if they volunteered to abandon much of their business.

A scarcely regulated food industry can engineer its products – loading them with fat, salt, sugar and high-fructose corn syrup – to bypass the neurological signals that would otherwise prompt people to stop eating. It can bombard both adults and children with advertising. It can (as we discovered yesterday) use the freedom granted to academy schools to sell the chocolate, sweets and fizzy drinks now banned from sale in maintained schools. It can kill off the only effective system (the traffic-light label) for informing people how much fat, sugar and salt their food contains. Then it can turn to the government and blame consumers for eating the products it sells. This is class war, a war against the poor fought by the executive class in government and industry.

We cannot yet state unequivocally that poor diet is a leading cause of Alzheimer’s disease, though we can say that the evidence is strong and growing. But if ever there was a case for the precautionary principle, here it is. It’s not as if we lose anything by eating less rubbish. Averting a possible epidemic of this devastating disease means taking on the bullies – both those who mock people for their pathology and those who spread the pathology by peddling a lethal diet.

Artificial butter flavoring ingredient linked to key Alzheimer’s disease process

Science Blog

A new study raises concern about chronic exposure of workers in industry to a food flavoring ingredient used to produce the distinctive buttery flavor and aroma of microwave popcorn, margarines, snack foods, candy, baked goods, pet foods and other products. It found evidence that the ingredient, diacetyl (DA), intensifies the damaging effects of an abnormal brain protein linked to Alzheimer’s disease. The study appears in ACS’ journal Chemical Research in Toxicology.

Robert Vince and colleagues Swati More and Ashish Vartak explain that DA has been the focus of much research recently because it is linked to respiratory and other problems in workers at microwave popcorn and food-flavoring factories. DA gives microwave popcorn its distinctive buttery taste and aroma. DA also forms naturally in fermented beverages such as beer, and gives some chardonnay wines a buttery taste. Vince’s team realized that DA has an architecture similar to a substance that makes beta-amyloid proteins clump together in the brain — clumping being a hallmark of Alzheimer’s disease. So they tested whether DA also could clump those proteins.

DA did increase the level of beta-amyloid clumping. At real-world occupational exposure levels, DA also enhanced beta-amyloid’s toxic effects on nerve cells growing in the laboratory. Other lab experiments showed that DA easily penetrated the so-called “blood-brain barrier,” which keeps many harmful substances from entering the brain. DA also stopped a protective protein called glyoxalase I from safeguarding nerve cells. “In light of the chronic exposure of industry workers to DA, this study raises the troubling possibility of long-term neurological toxicity mediated by DA,” say the researchers.