There’s more good news on the fish front: A large study conducted in developing countries found that a diet rich in fish may lower the risk of Alzheimer’s disease and other forms of dementia. And the more fish people ate, the less likely they were to develop the serious memory loss of dementia. The study adds to a growing body of evidence that a fish-rich diet may offer benefits for brain health.

Past research has suggested that eating fish may help to ward off dementia, but most of those studies were carried out in the United States other developed countries. Studies of people living in Italy, France and Spain who eat a traditional Mediterranean diet rich in fish as well as fruits and vegetables, for example, have shown that the diet may have brain-protective effects.

The findings are consistent with earlier reports that suggest that eating oily fish like tuna, salmon, mackerel, sardines and anchovies may help to keep the mind and memory sharp. Eating fish may also help to ease the agitation and depression of Alzheimers, other research shows.

Fish oils contain omega-3 fatty acids like EPA and DHA, which are known to be good for cardiovascular health. They also may help protect the brain against strokes and memory loss. DHA, or docosahexaenoic acid, and EPA, or eicosapentaenoic acid, are both thought to have disease-fighting properties.

In addition to fish, DHA and omega-3 dietary supplement pills are also widely available in pharmacies and health-food stores. Other foods high in these “good” fats include almonds, walnuts and many other types of nuts, as well as canola, walnut, soybean and flaxseed oils. Because many of these foods are a rich source of calories, however, it is best to eat them in place of, rather than in addition to, other foods.

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Understanding exactly how the brain encodes and stores memories is one of the central, unsolved mysteries in neuroscience. Currently the most widely accepted theory is long-term potentiation (LTP)—the lasting communication established between two neurons when they are stimulated simultaneously.

As a person processes an event, two neurons pass information through a small space called a synapse. This chemical conversation triggers an intricate cascade, inviting nearby neurons to fire and ultimately creating a network of connections with varying strengths. Afterward, this pattern of connections, or memory, remains within the network of neurons that processed the event.

Although many areas of the brain contain synapses capable of creating strong patterns of connectivity, the hippocampus is a particularly favorable spot for recording memories. This brain region plays a critical role in learning new information, forming spatial memories and storing short-term memories as long-term ones.

Memories formed with the hippo­campus are especially rich because they integrate input from several areas of the brain, and the ­hippocampus contains densely packed layers of neurons. In addition, damage to this region and nearby areas causes profound and perm­anent amnesia—an inability to store new memories or to recall old ones—and is observed in patients who have Alz­heimer’s disease.

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LONDON – Scientists have discovered a new source for the generation of nerve cells in the brain.

Professor Magdalena Gotz of Helmholtz Zentrum Munchen and Ludwig-Maximilians-Universitat (LMU) Munich and colleagues have discovered progenitor cells, which can form new glutamatergic neurons following injury to the cerebral cortex.

Particularly in Alzheimer’s disease, nerve cell degeneration plays a crucial role. In the future, new therapeutic options may possibly be derived from steering the generation and/or migration mechanism, according to the researchers.

Until only a few years ago, neurogenesis – the process of nerve cell development – was considered to be impossible in the adult brain.

Then researchers discovered regions in the forebrain in humans in which new nerve cells can be generated throughout life. These so-called GABAergic cells use gamma-aminobutyric acid (GABA), a neurotransmitter of the central nervous system.

Now, the research team, led by Gotz, has taken a closer look at this brain region in the mouse model. They found that even in the forebrain, there are other nerve cells that are regularly generated – the so-called glutamatergic nerve cells, which use glutamate as neurotransmitter.

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Australian scientists have confirmed what many chocoholics already know, that “comfort food” can reduce stress.

Eating foods rich in fat and sugar can alter the chemical composition of the brain and reduce anxiety, says Professor of Pharmacology Margaret Morris.

Prof Morris, from the University of NSW’s School of Medical Sciences, conducted a study of rats which showed the effects of past trauma could be erased through “unlimited access to yummy food”.

“Implementing that diet reversed their anxiety … it took an animal back to the non-stressed state,” Prof Morris told AAP.

“We really don’t know why that happens, but there seems to be a biochemical link.”

The research started with different groups of baby rats – one group grew up with normal contact with their mothers, while the other group had lengthy periods of separation.

Rats with a more traumatic early life were found to have higher levels of stress hormones and fewer steroid receptors in the part of the brain which controls behavior.

The signals for “anxiety and depression” eventually disappeared among those rats who were later switched to the all-you-can-eat junk food diet.

“The control group had no effect from the diet really, but the stressed animals had a deficit … which was restored by the diet.”

“(The) food seems to affect neurogenesis similar to the way anti-depressants promote nerve growth in the brain.”

Prof Morris cautioned while the results were not immediately transferable to people, it did show support “the therapeutic value of comfort food” and hint at explanations for other patterns of human behavior.

“If you ask people what they eat when they are stressed, they eat more chocolate, cakes and sweets, and less fish, vegetables and fruit,” she said.

And: “There is good evidence that if we look at people who have experienced trauma as a child tend to be heavier as adults”.

The study also should not be seen as an endorsement of eating junk food, Prof Morris said, noting this would set people on a path to other serious health problems.

Future research would aim to determine whether other rewarding activities – such as exercise – could have a similar stress-busting affect on rats’ brains.

The research was conducted jointly with PHD student Jayanthi Maniam, and it is published in the journal Psychoneuroendrocrinology.

Through the brain-imaging work at the Amen Clinics during the past 20 years with tens of thousands of people from 75 different countries, we have come to see that when your brain works right, you tend to be more thoughtful, playful, romantic, intimate, committed, and loving with your partner — all necessary things for great relationships.

When your brain has trouble, you are much more likely to be impulsive, distracted, addicted, unfaithful, angry, and even hateful — all things that undermine relationships.

Even though it feels genital, the vast majority of love and sex occurs in the brain. Your brain decides who is attractive to you, how to get a date, how well you do on a date, what to do with the feelings that develop, how long those feelings last, when to commit, and how well you do as a partner and parent. Your brain helps you be enthusiastic in the bedroom or drains you of desire and passion. Your brain helps you process and learn from a breakup or makes you vulnerable to depression or obsession.

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The ability of humans to learn, remember, and adapt is directly related to the changeableness (plasticity) of the human brain. Whenever we learn new information, the connections between nerve cells in the brain are modified. The activity of some connections (called synapses) increases, while the activity of other synapses decreases. The initial changes involve local chemical alterations in the way synapses transmit and receive information from other neurons. These initial chemical changes eventually lead to structural changes in the brain; that is, more connections and more complex connections form. The longer lasting of these changes require the turning on and turning off of specific genes; therefore, learning involves gene expression. Changes in synaptic connections represent a major way by which memories are formed. But some memories fade, and it is likely that the newly formed connections must be reinforced by ongoing brain activity in order for these connections to survive. The important points to remember are that learning alters the actual structure of the brain and that genes are involved in learning.

Neurogenesis

Neurogenesis (the formation of new nerve cells in the adult brain) is really part of the larger story about brain plasticity. Neurogenesis reflects the amazing resilience and plasticity of our brains. Expanding upon observations initially made years ago about birds, it has become clear that certain parts of the human brain are capable of generating new neurons throughout life, even during old age.  Not all regions of the brain appear to have this ability to grow new nerve cells, but two regions, the dentate gyrus of the hippocampus and the areas near the lateral ventricles in the olfactory system (which is involved in the sense of smell), are really good at it. The dentate gyrus plays a key role in the function of the hippocampus, the region that is so critical for memory processing. A thousand or more new neurons are born in this region each day and can be incorporated into the circuitry of the hippocampus where they help enhance certain types of learning. These new neurons may be particularly important for processing new information.

To make memories, new neurons must erase older ones

Short-term memory may depend in a surprising way on the ability of newly formed neurons to erase older connections. That’s the conclusion of a report in the November 13th issue of the journal Cell, a Cell Press publication, that provides some of the first evidence in mice and rats that new neurons sprouted in the hippocampus cause the decay of short-term fear memories in that brain region, without an overall memory loss.

The researchers led by Kaoru Inokuchi of The University of Toyama in Japan say the discovery shows a more important role than many would have anticipated for the erasure of memories. They propose that the birth of new neurons promotes the gradual loss of memory traces from the hippocampus as those memories are transferred elsewhere in the brain for permanent storage. Although they examined this process only in the context of fear memory, Inokuchi says he “thinks all memories that are initially stored in the hippocampus are influenced by this process.”

In effect, the new results suggest that failure of neurogenesis will lead to problems because the brain’s short-term memory is literally full. In Inokuchi’s words, we may perhaps experience difficulties in acquiring new information because the storage capacity of the hippocampus is “occupied by un-erased old memories.”

Of course, Inokuchi added, “our finding does not necessary deny the important role of neurogenesis in memory acquisition.” Hippocampal neurogenesis could have a dual role, he says, in both erasing old memories and acquiring new ones.

Earlier studies had shown a crucial role for the hippocampus in memorizing new facts. Studies in people with impaired and normal memories and in animals also showed that information recall initially depends on the hippocampus. That dependence progressively decays over time as memories are transferred to other regions, such as the neocortex. Scientists have also observed a similar decay in the strength of connections between neurons of the hippocampus, a phenomenon known as long-term potentiation (LTP) that is considered the cellular basis for learning and memory.

Scientists also knew that new neurons continue to form in the hippocampuses of adults, even into old age. But it wasn’t really clear what those newborn brain cells actually do. Inokuchi’s team suspected that the integration of new neurons was required to maintain neural connections, but they realized it might also go the other way. The incorporation of new neurons into pre-existing neural circuits might also disturb the structure of pre-existing information, and indeed that is what their new findings now show.

The researchers found that irradiation of rat’s brains, which drastically reduces the formation of new neurons, maintains the strength of neural connections in the hippocampus. Likewise, studies of mice in which hippocampal neurogenesis was suppressed by either physical or genetic means showed a prolonged dependence of fear memories on that brain region.

On the other hand, voluntary exercise, which causes a rise in the birth of new neurons, sped up the decay rate of hippocampus-dependency of memory, without any memory loss.

“Enhanced neurogenesis caused by exercise may accelerate memory decay from the hippocampus and at the same time it may facilitate memory transfer to neocortex,” Inokuchi said. “Hippocampal capacity of memory storage is limited, but in this way exercise could increase the [brain's overall] capacity.”

The study sets the stage for further examination of the connections between neurogenesis and learning capacity, the researchers say. They also plan to examine how the gradual decay of memory dependence on the hippocampus relates to the transformation of memory over time from a detailed and contextually-rich form to a more generic one.

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