When inflammation arises in the body as a result of infection or injury, the immune response also appears to accelerate memory loss in people with Alzheimer’s, according to a recent study published in the journal Neurology. In this study of changes in patients’ cognitive abilities over a span of six months, Alzheimer’s patients who had chronic (ongoing) inflammation as a result of, for instance, obesity or arthritis experienced four times the amount of memory loss as compared with patients without such inflammation. And those with chronic inflammation who also experienced an acute immune response (short-term, such as from an infection) were even worse off: their memory loss accelerated 10 times faster than patients without any inflammation.

“When we started the study, we thought short-lived events would be impor­tant,” says lead author Clive Holmes, a professor of biological psychiatry at the University of Southampton in England. “We hadn’t realized how important chronic inflammation was going to be.”

So how does inflammation, whether from an infection or from chronic dis­ease, damage the brain? The answer lies in the body’s immune response, which launches an attack on invading pathogens, releasing inflaming proteins such as tumor necrosis factor, or TNF. This molecule causes the vagus nerve, which extends from the brain to the abdomen and controls vital functions such as heartbeat, to send an electrical im­pulse to the brain, thereby directing the brain to secrete its own immune messengers.

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According to researchers from Finland and Sweden, people who live alone have twice the risk of developing dementia and Alzheimer’s disease in later life compared with married or cohabiting people.

Being widowed or divorced in mid-life carries three times the risk of developing dementia, says study author Miia Kivipelto.

As life expectancy increases in various regions of the world, dementia is becoming a growing health concern. In 2005 an estimated 25 million people had dementia, and the number is expected to reach 81.1 million by 2040. Alzheimer’s disease is the most common form of dementia and is the sixth-leading cause of death in the United States.

Dementia is a word for a group of symptoms caused by disorders that affect the brain. Memory loss is a common symptom of dementia. However, memory loss by itself does not mean you have dementia. People with dementia have serious problems with two or more brain functions, such as memory and language.

While there have been a number of studies linking being in a couple to good health and longevity this is the first study to focus on marital status and the risk of dementia.

The researchers interviewed a random sample of men and women derived from a group of 2000 adults. The participants came from two regions in Eastern Finland. They were initially surveyed at around 50 years of age and again around 21 years later. Participants were divided into the following groups: married/cohabitant, single, divorced or widowed. The team also investigated whether there was a link between living alone and being a carrier of the ApoE4 gene variant (or allele), the known genetic risk factor for Alzheimer’s.

The results reveal that people living without a partner during middle age had a higher risk of developing cognitive impairment in late life compared to those living with a partner. Individuals who become widowed at this age are three times more likely to develop dementia. The study also concluded that carriers of ApoE4 gene variant who lose their partners and remain living alone have the highest risk of developing Alzheimer’s disease.

These results are important for preventing dementia and cognitive impairment. As Kivipelto explains, we now know that it would be worth offering supportive intervention for individuals who have lost a partner.

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Researchers have shown for the first time that neural stem cells can rescue memory in mice with advanced Alzheimer’s disease, raising hopes of a potential treatment for the leading cause of elderly dementia that afflicts 5.3 million people in the U.S.

Dementia is a general term for a group of brain disorders that affect memory, judgment, personality and other mental functions. Alzheimer’s is the most common type of dementia, accounting for 60 to 80 percent of cases. There is currently no cure for Alzheimer’s.

Modified Alzheimer’s mice performed markedly better on memory tests a month after mouse neural stem cells were injected into their brains. The stem cells secreted a protein that created more neural connections, improving cognitive function.

“Essentially, the cells were producing fertilizer for the brain,” said Frank LaFerla, co-author of the study.

Lead author Mathew Blurton-Jones and colleagues worked with older mice predisposed to develop brains lesions called plaques and tangles that are the hallmarks of Alzheimer’s.

To learn how the stem cells worked, the scientists examined the mouse brains. To their surprise, they discovered that just 6 percent of the stem cells had turned into neurons. (The majority became the other two main types of brain cells, astrocytes and oligodendrocytes.) The stem cells didn’t improve cognition by becoming new neurons, nor did they act by reducing the number of plaques and tangles.

Rather, the stem cells were found to have secreted a protein called brain-derived neurotrophic factor, or BDNF. This caused existing tissue to sprout new neurites, strengthening and increasing the number of connections between neurons. When the team selectively reduced BDNF from the stem cells, the benefit was lost, providing strong evidence that BDNF is critical to the effect of stem cells on memory and neuronal function.

“If you look at Alzheimer’s, it’s not the plaques and tangles that correlate best with dementia; it’s the loss of synapses, connections between neurons,” Blurton-Jones said. “The neural stem cells were helping the brain form new synapses and nursing the injured neurons back to health.”

Diseased mice injected directly with BDNF also improved cognitively but not as much as with the neural stem cells, which provided a more long-term and consistent supply of the protein.

“This gives us a lot of hope that stem cells or a product from them, such as BDNF, will be a useful treatment for Alzheimer’s,” LaFerla said.

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Getting older is unavoidable, but falling apart mentally or physically is not. The biological mind-body connection becomes more important as you age. After all, a sound mind won’t do you much good if your body fails.

Loss of memory or cognitive decline shows up in the little things first. You have a harder time calling to mind the names of people and places, you have something at the tip of your tongue but just can’t remember what it is, you go into a room to get something and can’t remember what it was. The prefrontal cortex, which is your search engine for your memory, can’t call it up. Everyone has this happen at some point in their life. When this happens, the hippocampus kicks in to provide other associations to try to jog your memory, but those names and places which used to come easily become more difficult.

Brain-function research shows that as you age the cells throughout your body gradually lose their ability to adapt to stress. In the brain, when neurons get worn down from cellular stress, synapses erode, which eventually severs connections. Dendrites physically wither, and you start losing a signal here or there. Losing a signal here or there isn’t such a big deal at first, because the brain is designed to compensate by rerouting information around dead patches in the network and recruiting other areas to help with trafficking. The good news is your brain is a social network; it thrives on making new connections and is constantly rewiring itself and adapting – provided there’s enough stimulation to spur the growth of new neurons.

Memory is possible because of your neurons. Neurons are electrically excitable cells in the nervous system that process and transmit information. Neurons never actually touch each other. They reach toward each other across a gap (synapse) with their axons and dendrites (tiny hair-like filaments that project out).

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Until now, scientists have been uncertain exactly how Alzheimer’s disease kills brain cells, causing debate among researchers. The results of a new study show how amyloid plaques, found in the brain of Alzheimer’s patients, cause brain cells to die.

Researchers from University of Michigan and the University of California, San Diego were able to observe spikes in electrical currents across artificial cell membranes and in the membranes of live human cancer cells in the presence of the amyloid-beta peptide. What that told the scientists is that amyloid peptides poke holes in the cell membranes, allowing influx of calcium. Prior to the current research, it was believed that amyloid peptides thinned the cell membranes, producing calcium ion fluctuations. When ions become imbalanced, cell death results.
Want to know more? Read the rest of this article at: Alzheimer’s Disease Discovery

ScienceDaily (Apr. 18, 2009) — New therapeutic approaches in Alzheimer’s disease are urgently needed. Work led by Professor Mark Pepys FRS over more than 20 years has identified a protein known as serum amyloid P component (SAP) as a possible therapeutic target in Alzheimer’s disease. In collaboration with Roche he developed a new small molecule drug, CPHPC, which specifically targets SAP and removes it from the blood.

In the exciting new work reported now in the PNAS, the Pepys team together with Professor Martin Rossor and colleagues from the Dementia Research Centre of UCL’s Institute of Neurology, have shown that the drug also removes SAP from the brains of patients with Alzheimer’s disease.
Read the rest of this article by clicking the following link: Alzheimer’s Disease

Alzheimer’s disease is a 100-year-old myth that’s over the hill. So says Dr. Peter Whitehouse, a geriatric neurologist and author of “The Myth of Alzheimer’s: What You Aren’t Being Told About Today’s Most Dreaded Diagnosis.”

Whitehouse, who played an important role in brain research that led to the first four medications designed to treat Alzheimer’s, has replaced the term “Alzheimer’s disease” with “severe brain aging.” That distinction, he says, makes all the difference. He says we need to stop throwing money at searching for a cure to what he calls “age-associated cognitive challenges.” Instead of medication, the focus should be on preventing brain aging through simple strategies such as exercise, reading and eating right, he says.

We talked with Whitehouse ahead of his visit to the Twin Cities this week.

The interview with Dr. Whitehouse can be viewed at the following link: Brain Aging