by Meg Selig for Psychology Today:

You, like me, probably want to be “drop dead smart,” avoiding any adverse events or diseases that could damage your brain. But how can you keep your brain healthy, alert, and functioning optimally until the day you die?

Of course you have to feed your brain with healthy food, using sensible guidelines.  That’s a given. But the best brain food may not even be a food.  It could be an activity.

Is it learning a new language? Doing crossword puzzles? Having a mission in life? Calling a friend?  No, although these activities may be helpful to longevity, the key to brain health is something else. It’s regular exercise.

Evidence is piling up that suggests that mild to moderate aerobic exercise like brisk walking may protect your brain from the ravages of aging.  Here are summaries of a few recent research studies that link exercise with a healthy brain:

by Health Day News for Doctors Lounge:

For patients with dementia with Lewy bodies (DLB), treatment with 5 or 10 mg/day donepezil is associated with significant cognitive, behavioral, and global function improvements, according to research published in the July issue of the Annals of Neurology.

Etsuro Mori, M.D., Ph.D., of the Tohoku University Graduate School of Medicine in Sendai, Japan, and colleagues conducted a randomized, double-blind, placebo-controlled trial involving 140 patients with DLB who received either placebo or 3, 5, or 10 mg of donepezil hydrochloride per day for 12 weeks (35, 35, 33, and 37 patients, respectively).

Cognitive function was measured using the Mini-Mental State Examination (MMSE); behavioral changes were measured using the Neuropsychiatric Inventory; global function was evaluated using the Clinician’s Interview-Based Impression of Change-plus Caregiver Input (CIBIC-plus); and caregiver burden was also assessed.

by EurekAlert:

Study suggests that latrepirdine, which previously failed in clinical trials, may be successful if tested on patients with earlier stages of the disease.

An international team of scientists led by researchers at Mount Sinai School of Medicine have discovered that a drug that had previously yielded conflicting results in clinical trials for Alzheimer’s disease effectively stopped the progression of memory deterioration and brain pathology in mouse models of early stage Alzheimer’s disease. The findings, published July 31, 2012 in Molecular Psychiatry, demonstrate renewed potential for this compound and could lead to clinical trials in patients with early stages of the disease.

Latrepirdine, known commercially as Dimebon, was initially sold as an antihistamine in Russia, approved for use there in 1983. In the 1990s, researchers at the Institute of Physiologically Active Compounds in Moscow determined that the compound appeared effective in treating Alzheimer’s disease in animals.

by Judy Siegel-Itzkovich for Jerusalem Post:

‘V-Smart technology’ unique targeted drug delivery system could improve treatment of neurological diseases.

After eight years of intensive work, a team of Ben-Gurion University scientists has overcome the “blood brain barrier” that prevents drugs from passing into the brain and reaching specific targets to fight disease.

The system of synthetic nanoscale structures, called V-Smart drug delivery technology, also allows oral medications to pass through the epithelial tissue of the intestinal wall and other biological membranes; thus, the Beersheba researchers hope that injectable-only drugs for a variety of diseases could eventually be made in pill form.

by TDN Post:

by Science Daily:

During Alzheimer’s disease, ‘plaques’ of amyloid beta (Ab) and tau protein ‘tangles’ develop in the brain, leading to the death of brain cells and disruption of chemical signaling between neurons. This leads to loss of memory, mood changes, and difficulties with reasoning.

New research published in BioMed Central’s open access journal Alzheimer’s Research & Therapy, has found that up-regulating the gene Hes1 largely counteracted the effects of Ab on neurons, including preventing cell death, and on GABAergic signaling.

The exact mechanism behind how Ab contributes to Alzheimer’s disease is not yet fully understood, however researchers from Centro Andaluz de Biología Molecular y Medicina Regenerativa (CABIMER) in Spain recently discovered that Ab interferes with the normal activity of nerve growth factor (NGF). One of the actions of NGF is activating the protein Hes1, a transcription factor required to turn on other genes. Without this factor GABAergic signaling within the brain decreases.

by Medical XPress:

A study by scientists at the University of Southampton has revealed new clues to why people who carry the Alzheimer’s risk gene APOE4 may be more likely to develop the disease.

The findings, which link the risk gene to clearance of the hallmark Alzheimer’s protein amyloid, take scientists a step further towards understanding the devastating disease.

The research, published on July 25 in the journal PLoS ONE, was funded by Alzheimer’s Research UK.

The APOE gene is the biggest known genetic risk factor for late-onset Alzheimer’s disease. People who carry the APOE4 version of the gene have a higher risk of developing the disease at an earlier age than people who carry APOE3 or APOE2. However, the reason for this increased risk has remained unclear.

by Lisa Feierstein RN for Active Healtcare Inc.:

Quality sleep can prevent dementia according to a new study from the Brigham and Women’s Hospital in Boston. This two-year study (2002-2004) took 298 older women with an average age of 82 and determined if their later diagnosed dementia was caused by sleep apnea.

At the time of the study none of the participants had dementia. The study ultimately found a tie between sleep apnea and dementia: the women who had sleep apnea shared a 85 percent higher risk of developing dementia than those who had normal breathing.

The study also found that 60 percent of elderly men and women have some kind of sleep disorder, which can cause future dementia. What if we can reduce this number with more awareness? What if we can reduce the number of elderly in long-term nursing care? What if we can give the elderly more quality years with their children and grandchildren?

by Drew Ramsey M.D. for Huffington Post:

In my practice of psychiatric medicine, I spend every day treating patients so that their master mood regulator — the brain — will get more of what it needs to be strong, healthy, and happy.

But when I meet new patients, I know that the way most of them eat — the typical American diet of sugars, refined carbohydrates and industrial vegetable fats — does no favors for their mental health. The nation’s epidemic levels of obesity and diabetes have received plenty of news coverage, but rates of brain disorders like depression and dementia are also skyrocketing, and the American diet is partly to blame.

Why? Because so many of the nutrients that the human brain relies upon for its growth, healing and healthy functioning have been stripped from the food supply by modern food processing and factory farming. As a result, we as a nation are overfed and undernourished. We’re also being poisoned. Preservatives, pesticides and plastic packaging have introduced a slew of new chemicals into our systems, which pose additional threats to our brain functions.

by Michael Slezak for New Scientist:

Despite the fact that women live longer than men, their brains seems to age faster. The reason? Possibly a more stressful life.

When people age, some genes become more active while others become less so. In the human brain, these changes can be observed through the “transcriptome” – a set of RNA molecules that indicate the activity of genes within a population of cells.

When Mehmet Somel, a computational biologist at the University of California, Berkeley, and his colleagues compared the transcriptome of 55 male and female brains of different ages, they were surprised to find that the pattern of gene activation and deactivation that occurs with ageing appeared to progress faster in women than in men. This was particularly apparent in an area of the pre-frontal cortex.