WHAT: National Institutes of Health (NIH) scientists investigating how prion diseases destroy the brain have observed a new form of the disease in mice that does not cause the sponge-like brain deterioration typically seen in prion diseases. Instead, it resembles a form of human Alzheimer’s disease, cerebral amyloid angiopathy, that damages brain arteries.

The study results, reported by NIH scientists at the National Institute of Allergy and Infectious Diseases (NIAID), are similar to findings from two newly reported human cases of the prion disease Gerstmann-Straussler-Scheinker syndrome (GSS). This finding represents a new mechanism of prion disease brain damage, according to study author Bruce Chesebro, M.D., chief of the Laboratory of Persistent Viral Diseases at NIAID’s Rocky Mountain Laboratories.

Prion diseases, also known as transmissible spongiform encephalopathies, primarily damage the brain. Prion diseases include mad cow disease or bovine spongiform encephalopathy in cattle; scrapie in sheep; sporadic Creutzfeldt-Jakob disease (CJD), variant CJD and GSS in humans; and chronic wasting disease in deer, elk and moose.

The role of a specific cell anchor for prion protein is at the crux of the NIAID study. Normal prion protein uses a specific molecule, glycophosphoinositol (GPI), to fasten to host cells in the brain and other organs. In their study, the NIAID scientists genetically removed the GPI anchor from study mice, preventing the prion protein from fastening to cells and thereby enabling it to diffuse freely in the fluid outside the cells.

The scientists then exposed those mice to infectious scrapie and observed them for up to 500 days to see if they became sick. The researchers documented signs typical of prion disease including weight loss, lack of grooming, gait abnormalities and inactivity. But when they examined the brain tissue, they did not observe the sponge-like holes in and around nerve cells typical of prion disease. Instead, the brains contained large accumulations of prion protein plaques trapped outside blood vessels in a disease process known as cerebral amyloid angiopathy, which damages arteries, veins and capillaries in the brain. In addition, the normal pathway by which fluid drains from the brain appeared to be blocked.

Their study, Dr. Chesebro says, indicates that prion diseases can be divided into two groups: those with plaques that destroy brain blood vessels and those without plaques that lead to the sponge-like damage to nerve cells. Dr. Chesebro says the presence or absence of the prion protein anchor appears to determine which form of disease develops.

The new mouse model used in the study and the two new human GSS cases, which also lack the usual prion protein cell anchor, are the first to show that in prion diseases, the plaque-associated damage to blood vessels can occur without the sponge-like damage to the brain. If scientists can find an inhibitor for the new form of prion disease, they might be able to use the same inhibitor to treat similar types of damage in Alzheimer’s disease, Dr. Chesebro says.

Older people who have “mental lapses,” or times when their thinking seems disorganized or illogical or when they stare into space, may be more likely to have Alzheimer’s disease than people who do not have these lapses, according to a study published in the January 19, 2010, print issue of Neurology®, the medical journal of the American Academy of Neurology.

These mental lapses, also called cognitive fluctuations, are common in a type of dementia called dementia with Lewy bodies, but researchers previously did not know how frequently they occurred in people with Alzheimer’s disease and, equally important, what effect fluctuations might have on their thinking abilities or assessment scores.

The study involved 511 people with an average age of 78. Researchers interviewed the participant and a family member, evaluated the participants for dementia and tested their memory and thinking skills.

People with three or four of the following symptoms met the criteria for having mental lapses:

– Feeling drowsy or lethargic all the time or several times per day despite getting enough sleep the night before

– Sleeping two or more hours before 7 p.m.

– Having times when the person’s flow of ideas seems disorganized, unclear, or not logical — Staring into space for long periods

A total of 12 percent of the people with dementia in the study had mental lapses. Of 216 people with very mild or mild dementia, 25 had mental lapses. Of the 295 people with no dementia, only two had mental lapses.

Those with mental lapses were 4.6 times more likely to have dementia than those without mental lapses. People with mental lapses also tended to have more severe Alzheimer’s symptoms and perform worse on tests of memory and thinking skills than people who did not have lapses.

“When older people are evaluated for problems with their thinking and memory, doctors should consider also assessing them for these mental lapses,” said senior study author James E. Galvin.

Cognitive fluctuations, or episodes when train of thought temporarily is lost, are more likely to occur in older persons who are developing Alzheimer’s disease than in their healthy peers, according to scientists at Washington University School of Medicine in St. Louis.

Cognitive fluctuations include excessive daytime sleepiness, staring into space and disorganized or illogical thinking.

“If you have these lapses, they don’t by themselves mean that you have Alzheimer’s,” says senior author James Galvin, M.D., a Washington University neurologist at Barnes-Jewish Hospital. “Such lapses do occur in healthy older adults. But our results suggest that they are something your doctor needs to consider if he or she is evaluating you for problems with thinking and memory.”

The study appears in the Jan. 19 issue of Neurology.

Earlier research had associated cognitive fluctuations with another form of dementia called dementia with Lewy bodies, but little information existed on the potential for links between Alzheimer’s and such lapses.

Data for the new study came from Alzheimer’s disease evaluations of 511 older adults with memory problems. Average age of the participants was 78. Researchers gave participants standard tests of thinking and memory skills. They also interviewed participants and a family member, checking for prolonged daytime sleepiness, drowsiness or lethargy in spite of sufficient sleep the night before, periods of disorganized or illogical thinking, or instances of staring into space for long periods of time.

A total of 12 percent of the participants had at least three of these symptoms, meeting the criteria for cognitive fluctuations. Those with mental lapses were 4.6 times more likely to be diagnosed with Alzheimer’s. Of 216 diagnosed with very mild or mild dementia, 25 had mental lapses; of the 295 with no dementia, only two had mental lapses. In addition, participants with mental lapses did worse on tests of memory and thinking than people without mental lapses.

“We have some ideas about why the biology of dementia with Lewy bodies causes these mental lapses, but nothing comparable for Alzheimer’s,” Galvin says. “It’s possible that some of the patients who were diagnosed with Alzheimer’s disease in this study will go on to develop dementia with Lewy bodies, but at the time of the study, they weren’t showing any of the Lewy body dementia’s core features.”

Lewy body dementia, which causes clumps of proteins known as Lewy bodies to form in neurons, is thought to be the second most common form of dementia after Alzheimer’s. Clinically, it can overlap with Parkinson’s disease and Alzheimer’s disease. Pronounced cognitive fluctuations are a hallmark of Lewy body dementia, as are visual hallucinations and rapid eye movement behavior sleep disorder.

First it was exercise on prescription, then it was arts on prescription, soon it could be singing on prescription, as the clinical evidence builds up, and as more and more projects promote the benefits of singing to health and wellbeing, both for those in generally good health and those with physical and mental health problems, or who find themselves socially excluded or isolated.

Consider this scenario: you go to your doctor and instead of coming away clutching a prescription for a bottle of pills or a referral to a counsellor, you have a leaflet about a local singing group. This is the vision of Grenville Hancox MBE, Director of the Sidney De Haan Research Centre for Arts and Health based at Canterbury Christ Church University in the UK.

Imagine the day, says Hancox, when your GP says: “Go and have a sing with that lot down the road” instead of “take these pills three times a day!”

Exercise on prescription schemes have been gaining ground all across the UK over the last decade, to the point where there are now national standards for GP exercise referral schemes. And more recently, Arts on prescription appeas to be growing too, as exemplified with projects by Healing Arts on the Isle of Wight (Time Being) and East Kent Health Promotion Department.

But the idea that involvement in group singing can benefit health and wellbeing is also growing; the Sidney De Haan Research Centre lists several established projects:

* Singing for the Brain, East Berkshire Alzheimer’s Society.
* Sing Your Heart Out, Hellesdon Hospital, Norwich
* Serendipity Singing for Health Choir, Midlothian
* Singing is Good for You, Voices Foundation
* Singing Medicine, Birmingham Children’s Hospital
* Sounds Lively Choir, Isle of Wight

And at Sidney De Haan they are also working on “providing a convincing rationale” for a practical scheme for Singing on Prescription that “can be tested for its effectiveness through controlled evaluation”, according to a statement on their website.

Chreanne Montgomery-Smith, a support and development officer with the West Berkshire branch of the Alzheimer’s Society founded Singing for the Brain in 2002.

She wrote in 2006 in the Journal of Dementia Care she believed there were seven therapeutic outcomes from singing in a group that were of particular benefit to people with Alzheimer’s, although one can see how these might apply to people in many other situations too:

* Communication: the singing warm up (exercises involving whole body, neck, shoulders, jaw, face, lips, tongue, diaphragm) strengthen neural connections to the voice and breath, and doing them in a group is fun and non-threatening compared to doing it one-to-one.

* Cognition: singing challenges concentration and attention, especially when techniques such as singing from memory, combining rhythm with action, and mental substitution are used.

* Engagement: for example making eye contact across the group and expressing to the audience the emtional message of a song.

* Confidence: joining a singing group can build confidence from the gradual gaining of skills, vocal strength and the thrill of being able to remember so much. Fear of failure is lessened when everyone is in the same situation and group members laugh together when they make mistakes.

* Relationships: in a group with a shared purpose and a leader that treats everyone equally, there is a chance to get away from those situations where you are a person with a condition, and relate to people in a different way. You make friends, find and give support, and express frustrations and emotions about relationship problems in many songs that cover those areas of life (Montgomery-Smith gives the example of “A Fine Romance” as a “safe” way to express one’s frustration with a life partner).

* Empowerment: by leading singing rounds, taking responsibility for setting out chairs, getting scores ready, writing lyrics, greeting new members, there is a wide range of roles that help people feel more in charge of themselves and their lives and what they contribute to a group. Former carers also benefit: giving them a new role when they have lost a major one.

* Exercise and stress reduction: an excellent way to reduce stress is learning to exhale; it increases circulation as the diaphragm massages internal organs. It releases endorphins and improves the immune response, according to research that showed immune system changes in salivary Immunoglobulin A and Cortisol.
Dr Nicholas Hopkinson, who is leading the study at the Royal Brompton, said the study was trialling a novel approach with teaching breathing techniques. Often, when you try to teach a patient directly, they become even more conscious of the need to breath correctly, and this can make things worse, he said.

By learning to sing, the patients are being approached more “from the side”, said Hopkinson, they are learning to “use their voice and their breathing for a different purpose, for singing, hoping that the skills that they gain through that in terms of controlling their breathing will actually be helpful in day-to-day life,” he told the BBC.

Voice trainer Phoene Cave said she saw improvements in breathing control after just one session.

“I’m helping them to become aware of their bodies in a way that they’re not used to,” she told the BBC.

The class always starts with vocal exercises, including collective sighing, buzzing noises, and making “ha-ha” sounds up and down the scales.

Research suggests that regular singing practice also helps people with dyspnea, improves mood and reduces depression.

John Townsend, a patient in the Royal Brompton and member of the singing group, said that the evidence was plain to see. He explained how when they start their lessons, people from the wards just come along and join in:

“You can hear it all the way along the wards. And people are cheerful.”

“They become cheerful and they’re not even singing. So of course it’s a great thing,” said Townsend.

High blood pressure may put women at greater risk for dementia later in life by increasing white matter abnormalities in the brain, report researchers from the University of Pittsburgh Graduate School of Public Health in a study published online in the Journal of Clinical Hypertension.

“Hypertension is very common in the U.S. and many other countries, and can lead to serious health problems,” said Lewis Kuller, M.D., Dr.P.H., professor of epidemiology, University of Pittsburgh Graduate School of Public Health. “Proper control of blood pressure, which remains generally poor, may be very important to prevent dementia as women age.”

The study, part of the multisite and long-term Women’s Health Initiative Memory Study (WHIMS), included 1,424 women 65 or older who had their blood pressure assessed annually and underwent magnetic resonance imaging (MRI) of the brain. Researchers assessed white matter lesions, which are associated with increased risks for dementia and stroke. White matter makes up 60 percent of the brain and contains nerve fibers responsible for communication among the brain’s regions.

Women who, at the start of the study, were hypertensive, meaning a blood pressure of 140/90 or higher, had significantly more white matter lesions on their MRI scans eight years later than participants with normal blood pressure. Lesions were more common in the frontal lobe, the brain’s emotional control center and home to personality, than in the occipital, parietal or temporal lobes.

“Women should be encouraged to control high blood pressure when they are young or in middle-age in order to prevent serious problems later on,” said Dr. Kuller. “Prevention and control of elevated blood pressure and subsequent vascular disease in the brain may represent the best current preventive therapy for dementia.”

We all have at one time or another experienced the typical signs of an infection: the fever, the listlessness, the lack of appetite. They are orchestrated by the brain in response to circulating cytokines, the signaling molecules of the immune system. But just how cytokines’ reach extends beyond the almost impenetrable blood-brain barrier has been the topic of much dispute.

In their latest study, researchers at the Salk Institute for Biological Studies describe how, depending on the nature of the stimulus, resident macrophages lined up along the blood-brain barrier play opposing roles in the transmission of immune signals into the brain.

“These macrophages act as accelerators to enlist the brain’s participation in dealing with immune insults, but when necessary slam on the brakes to prevent the central inflammatory response from going overboard,” explains postdoctoral researcher Jordi Serrats, Ph.D., who co-led the study with Jennifer C. Schiltz, Ph.D., formerly a postdoctoral researcher in the Salk’s Neuronal Structure and Function Laboratory and now an assistant professor at the Uniformed Services University in Bethesda, Maryland.

The Salk researchers’ findings, which are published in the Jan. 14, 2010 edition of the journal Neuron, may pave the way for novel therapies for sufferers of chronic neurodegenerative diseases, such as Amyotrophic Lateral Sclerosis (ALS), Parkinson’s, Alzheimer’s and prion diseases, in which central inflammatory mechanisms play an important role.

“The fact that we have identified a potent anti-inflammatory mechanism in the brain presents a new target to intervene in the wide range of central nervous system diseases that possess an inflammatory component,” says the study’s senior author, Paul E. Sawchenko, Ph.D., a professor in the Neuronal Structure and Function Laboratory.

In response to an infection, inflammatory cytokines such as interleukin-1 are generated at the site of infection. These cytokines circulate in the blood and communicate with neurons in the brain to engage the hypothalamo-pituitary-adrenal (HPA) axis, an integral part of the brain’s stress response machinery. The HPA axis involves the interaction of the hypothalamus, the pituitary gland, which sits just below the hypothalamus and the adrenal glands at the top of the kidneys.

Like a central command center, the hypothalamus sends out corticotropin-releasing factor, which stimulates the pituitary gland to secrete adrenocorticotropic hormone. The latter signals the adrenal glands to ramp up the production of glucocorticoids, which mobilize energy reserves to cope with inflammatory insults. But they also act as very powerful immunosuppressants preventing excessive cytokine production and immune cell proliferation.

“Cytokines are big molecules that don’t cross the blood-brain barrier freely,” says Sawchenko. “The question of how these molecules access the brain to trigger this whole array of adaptive responses such as fever, inactivity, sleepiness, and activation of the brain’s stress response machinery has been a nagging problem in the side of neuroimmunology for many years.”

Earlier research by Sawchenko and others suggested a vascular route whereby cytokines interact with vessel walls to generate secondary messengers, which then engage the relevant circuitry in the brain. Tightly packed endothelial cells, which line almost 400 miles of narrow capillaries throughout the brain, are perfectly positioned to record circulating immune signals but they require a very strong signal to become activated. Perivascular macrophages, on the other hand, are more sensitive but don’t have direct access to the bloodstream.

To disentangle the exact role of these two cell types, Serrats took advantage of the macrophages’ ability to engulf and ingest solid particles. He injected liposomes containing clodronate, a drug that can cause cell death, into the lateral cerebral ventricle. The liposomes were taken up by the macrophages, which were selectively killed off.

Without perivascular macrophages, the animals were unable to respond to blood-borne interleukin-1 and initiate the brain’s so-called acute phase responses, which help the body deal with the challenge at hand but also cause the familiar feeling of “being sick.” But to their surprise, the Salk researchers found that the same cells put a damper on the pro-inflammatory activities of endothelial cells, which form the lining of blood vessels and are only stirred to action-but very powerfully once they are-when they encounter lipopolysaccharide, a key component of the cell wall of certain bacteria.

“Many neurodegenerative diseases are worsened by systemic inflammation or infections,” says Sawchenko. “Once we identify the molecules that mediate the two-way communication between perivascular macrophages and endothelial cells we can develop strategies for managing the adverse health consequences of central inflammatory responses.”

Research published today on bmj.com reports that angiotensin receptor blockers are associated with a reduced risk of Alzheimer’s disease and dementia. These drugs are normally used to treat high blood pressure and heart disease.

In addition, the study concludes that angiotensin receptor blockers appear to offer greater protection against Alzheimer’s disease and dementia than other high blood pressure and heart disease medication.

A growing number of people are threatened by dementia (including Alzheimer’s disease) as they get older. This has important economic implications since individuals who suffer from either disease can spend long periods of time in nursing homes.

Dementia and Alzheimer’s disease are complex diseases. There is increasing evidence of three main risk factors:

• age
• genetics
• heart disease

Mid-life diseases particularly like diabetes and high blood pressure seem to be associated with a higher chance of developing dementia.

Researchers explain that this is the first large scale study to investigate whether angiotensin receptor blockers reduce the risk of developing dementia and Alzheimer’s disease.

Professor Benjamin Wolozin from Boston University School of Medicine led the team of researchers. They investigated the incidence of dementia in over 800,000 individuals in the US from 2002 to 2006. They were mostly (98 percent) male subjects. The participants had cardiovascular disease and were 65 years of age or older.

The research subjects were divided in three groups: one using angiotensin receptor blockers, another the blood pressure lowering drug lisinopril and the third using other comparative drugs used for heart disease.

The findings indicate that the group on angiotensin receptor blockers was significantly less likely to develop Alzheimer’s disease or dementia. In addition, they reveal that angiotensin receptor blockers have an additive effect when used in combination with another type of high blood pressure drug (ACE inhibitors). In fact, individuals with existing Alzheimer’s disease or dementia who took both medicines were less likely to die early or be admitted to nursing homes.

In conclusion, Wolozin comments that the research is significant because it is the “first to compare both risk of dementia and progression of dementia in users of angiotensin receptor blockers compared with users of a drug from the same class (lisinopril) or users of other drugs prescribed for cardiovascular disease.”

In an associated editorial, two senior doctors from the University of Calgary highlight that the public health implications of finding an effective way of preventing dementia are immense. They say in closing that however, further work is needed to verify the usefulness of antihypertensives in general and angiotensin receptor blockers in particular.

“Use of angiotensin receptor blockers and risk of dementia in a predominantly male population: prospective cohort analysis”

Forgot where you put your car keys? Having trouble recalling your colleague’s name? If so, this may be a symptom of subjective cognitive impairment (SCI), the earliest sign of cognitive decline marked by situations such as when a person recognizes they can’t remember a name like they used to or where they recently placed important objects the way they used to. Studies have shown that SCI is experienced by between one-quarter and one-half of the population over the age of 65. A new study, published in the January 11, 2010, issue of the journal Alzheimer’s & Dementia, finds that healthy older adults reporting SCI are 4.5 times more likely to progress to the more advanced memory-loss stages of mild cognitive impairment (MCI) or dementia than those free of SCI.

The long-term study completed by researchers at NYU Langone Medical Center tracked 213 adults with and without SCI over an average of seven years, with data collection taking nearly two decades. Further cognitive decline to MCI or dementia was observed in 54 percent of SCI persons, while only in 15 percent of persons free of SCI.

“This is the first study to use mild cognitive impairment as well as dementia as an outcome criterion to demonstrate the outcome of SCI as a possible forerunner of eventual Alzheimer’s disease,” said Barry Reisberg, MD, professor of psychiatry, director of the Fisher Alzheimer’s Disease Program and director, Clinical Core, NYU Alzheimer’s Disease Center at NYU Langone Medical Center. “The findings indicate that a significant percentage of people with early subjective symptoms may experience further cognitive decline, whereas few persons without these symptoms decline. If decline does occur in those without SCI symptoms, it takes considerably longer than for those with subjective cognitive symptoms.”

According to the authors, scientists and physicians can now target the prevention of eventual Alzheimer’s disease in the SCI stage, beginning more than 20 years before dementia becomes evident

“These intriguing results more fully describe the possible relationship between early signs of memory loss and development of more serious impairment. This is critical to know, as we look for ways to define who is at risk and for whom the earliest interventions might be successful,” said Neil Buckholtz, PhD, National Institute on Aging (NIA) which supported the research. “These findings also underscore the importance of clinicians’ asking about, and listening to, concerns regarding changes in cognition and memory among their aging patients.”

An international team of researchers studying the long term effects of electromagnetic waves like those emitted by cell phones on mice were surprised to find they protected their brains against Alzheimer’s and even reversed the memory damage caused by the disease.

The study was the work of neuroscientists, electrical engineers, and neurologists from universities in the US, Japan and China, and is being published online on 7 January in the Journal of Alzheimer’s Disease. The study was led by University of South Florida (USF) researchers at Florida’s Alzheimer’s Disease Research Center (ADRC), a statewide project sponsored by the National Institute on Aging.

One of the hallmarks of Alzheimer’s disease is the accumulation of sticky deposits or plaques of beta-amyloid protein in the brain.

While it is not clear what role plaques play in Alzheimer’s, many experts believe they stop brain cells communicating with each other and also disrupt other processes that cells rely on to survive. Most treatments for Alzheimer’s try to target beta-amyloid protein.

In this study, researchers took mice genetically engineered to develop symptoms of Alzheimer’s disease, exposed them to cell phone waves and discovered the electromagnetic radiation prevented build up of amyloid protein in the brains of young mice, erased deposits of the protein in the brains of old Alzheimer’s mice, and also reversed memory damage.

Lead author of the study, USF research professor Dr Gary Arendash told the press that:

“It surprised us to find that cell phone exposure, begun in early adulthood, protects the memory of mice otherwise destined to develop Alzheimer’s symptoms.”

“It was even more astonishing that the electromagnetic waves generated by cell phones actually reversed memory impairment in old Alzheimer’s mice.”

A USF statement describes the study as “highly-controlled”: the researchers were able to isolate the effects of cell phone exposure from other lifestyle factors like diet and exercise.

For the study the researchers used 96 mice, most of which where genetically altered to develop beta-amyloid plaques and memory problems mimicking Alzheimer’s disease as they got older (the “Alzheimer’s mice). The others were not genetically engineered in this way and acted as controls (the “normal” mice).

The researchers exposed both groups of mice: the ones genetically predisposed to develop Alzheimer’s and the normal controls, to an electromagnetic field like that generated by standard cell phones for two periods lasting one hour each every day for between seven and nine months.

To achieve this effect the researchers arranged the animals’s cages in a circle around an antenna generating the cell phone signal. All the animals were kept at the the same distance from the antenna and exposed to electromagnetic waves typically emitted by a cell phone pressed up against a human head, said the USF researchers in a statement.

The results showed that:

* Exposure started when they were young adults, ie before showing signs of memory impairment, appeared to protect the Alzheimer’s mice from becoming cognitively impaired.

* Exposed older Alzheimer’s mice performed as well on tests measuring memory and thinking skills as normal older mice without dementia.

* When older, previously unexposed Alzheimer’s mice already showing memory problems were exposed to the electromagnetic field, their memory impairment vanished.

* Normal mice exposed to the electromagnetic waves for several months showed above normal memory performance.

To assess the mice’s memory skills, the researchers adapted a test designed to assess mild cognitive impairment in humans.

“Since we selected electromagnetic parameters that were identical to human cell phone use and tested mice in a task closely analogous to a human memory test, we believe our findings could have considerable relevance to humans, said Arendash.

It took several months for the effects of the electromagnetic wave exposure to show in the mice: this suggests it would take years in humans.

Arendash and colleagues concluded that electromagnetic field exposure could be an effective, drug-free, non-invasive way to prevent and treat Alzheimer’s disease in humans.

They are now investigating the effect of different frequencies and strengths of electromagnetic radiation: eg will it be more or less rapid, and will the cognitive benefits be greater or less, than they found in this study.

Co-author of the study and major member of the USF team, Dr Chuanhai Cao, said:

“If we can determine the best set of electromagnetic parameters to effectively prevent beta-amyloid aggregation and remove pre-existing beta amyloid deposits from the brain, this technology could be quickly translated to human benefit against AD [Alzheimer's disease]“.

“Since production and aggregation of beta-amyloid occurs in traumatic brain injury, particularly in soldiers during war, the therapeutic impact of our findings may extend beyond Alzheimer’s disease,” said Cao.

When they monitored the mice during their one-hour exposures when the electromagnetic field was turned on, the researchers noticed that after several months, the brain temperature of the Alzheimer’s mice rose slightly; this did not happen in the normal mice.

Speculating on this observation in the light of the other results, the researchers suggest perhaps the temperature increase helped brain cells to release the newly-formed beta-amyloid plaques.

As an explanation for the improved memory function in the normal mice after months of exposure, they suggested perhaps the electromagnetic waves increased brain activity by boosting blood flow and energy metabolism in the brain.

“Our study provides evidence that long-term cell phone use is not harmful to brain,” said Cao, adding that:

“To the contrary, the electromagnetic waves emitted by cell phones could actually improve normal memory and be an effective therapy against memory impairment.”

Arendash said it will be a while yet before we know exactly what is going on: how the waves produce these beneficial effects on memory. But one thing is clear he said:

“The cognitive benefits of long-term electromagnetic exposure are real, because we saw them in both protection- and treatment-based experiments involving Alzheimer’s mice, as well as in normal mice.”

There may be a new effective way to prevent and treat Alzheimer’s disease on the horizon, through raising levels of the hormone leptin. Alzheimer’s is the most common cause of a declining mental state that affects how well someone can speak, process thoughts and carry out their daily activities. Researchers continue to search for the right treatment and prevention for the disease.

The new discovery is connected to the energy regulating hormone leptin, which was discovered in the 1990s. Leptin is produced by fat cells and is thought to play a key role in controlling hunger and weight. There is now growing evidence linking leptin to brain development and memory. The new study evaluating leptin levels and its effects on Alzheimer’s disease, recently released in the Journal of the American Medical Association and conducted at Boston University Medical Center, involved patients that began in 1948 with the Framington Heart Study, and included 785 elderly volunteers originally. Between 1990 and 1994 levels of blood leptin levels were checked in the volunteers, and around eight years later there were regular brain scans conducted on 198 older volunteers that had not developed dementia, to check how their brains had aged.

Through the study there is evidence showing those with higher levels of leptin had four times better odds of not developing Alzheimer’s disease than those with much lower levels of the hormone. Patients beginning the study with higher leptin levels were rewarded with healthier brains and fewer signs of aging. A fourth of those with the lower levels of leptin eventually developed Alzheimer’s disease compared to only 6 percent of the participants that reported the highest leptin levels.

The newly released study was an additional step to study the effects of leptin in Alzheimer’s patients since there have been evidence linking leptin levels to brain plaques in patients with Alzheimer’s. There is more research in regards to leptin on the way. A small pilot study, being funded by a $3 million award from the National Institutes of Health, to study leptin replacement therapy’s affects on Alzheimer’s patients, will be recruiting 45 patients soon.

The researchers of the newly released study said, “If our findings are confirmed by others, leptin levels in older adults may serve as one of several possible biomarkers for healthy brain aging and, more importantly, may open new pathways for possible preventative and therapeutic interventions.” Studies involving animals and leptin treatment have shown memory performance improvements even after signs of Alzheimer’s have began. However, lead researcher Sudha Seshadri, M.D., of Boston University School of Medicine says it remains to be seen if leptin replacement therapy will benefit Alzheimer’s patients or help to prevent the onset of the disease.