Posts Tagged ‘neurodegeneration’

by Emily Mullin

When David Graham wakes up in the morning, the flat white box that’s Velcroed to the wall of his room in Robbie’s Place, an assisted living facility in Marlborough, Massachusetts, begins recording his every movement.

It knows when he gets out of bed, gets dressed, walks to his window, or goes to the bathroom. It can tell if he’s sleeping or has fallen. It does this by using low-power wireless signals to map his gait speed, sleep patterns, location, and even breathing pattern. All that information gets uploaded to the cloud, where machine-learning algorithms find patterns in the thousands of movements he makes every day.

The rectangular boxes are part of an experiment to help researchers track and understand the symptoms of Alzheimer’s.

It’s not always obvious when patients are in the early stages of the disease. Alterations in the brain can cause subtle changes in behavior and sleep patterns years before people start experiencing confusion and memory loss. Researchers think artificial intelligence could recognize these changes early and identify patients at risk of developing the most severe forms of the disease.

Spotting the first indications of Alzheimer’s years before any obvious symptoms come on could help pinpoint people most likely to benefit from experimental drugs and allow family members to plan for eventual care. Devices equipped with such algorithms could be installed in people’s homes or in long-term care facilities to monitor those at risk. For patients who already have a diagnosis, such technology could help doctors make adjustments in their care.

Drug companies, too, are interested in using machine-learning algorithms, in their case to search through medical records for the patients most likely to benefit from experimental drugs. Once people are in a study, AI might be able to tell investigators whether the drug is addressing their symptoms.

Currently, there’s no easy way to diagnose Alzheimer’s. No single test exists, and brain scans alone can’t determine whether someone has the disease. Instead, physicians have to look at a variety of factors, including a patient’s medical history and observations reported by family members or health-care workers. So machine learning could pick up on patterns that otherwise would easily be missed.


David Graham, one of Vahia’s patients, has one of the AI-powered devices in his room at Robbie’s Place, an assisted living facility in Marlborough, Massachusetts.

Graham, unlike the four other patients with such devices in their rooms, hasn’t been diagnosed with Alzheimer’s. But researchers are monitoring his movements and comparing them with patterns seen in patients who doctors suspect have the disease.

Dina Katabi and her team at MIT’s Computer Science and Artificial Intelligence Laboratory initially developed the device as a fall detector for older people. But they soon realized it had far more uses. If it could pick up on a fall, they thought, it must also be able to recognize other movements, like pacing and wandering, which can be signs of Alzheimer’s.

Katabi says their intention was to monitor people without needing them to put on a wearable tracking device every day. “This is completely passive. A patient doesn’t need to put sensors on their body or do anything specific, and it’s far less intrusive than a video camera,” she says.

How it works

Graham hardly notices the white box hanging in his sunlit, tidy room. He’s most aware of it on days when Ipsit Vahia makes his rounds and tells him about the data it’s collecting. Vahia is a geriatric psychiatrist at McLean Hospital and Harvard Medical School, and he and the technology’s inventors at MIT are running a small pilot study of the device.

Graham looks forward to these visits. During a recent one, he was surprised when Vahia told him he was waking up at night. The device was able to detect it, though Graham didn’t know he was doing it.

The device’s wireless radio signal, only a thousandth as powerful as wi-fi, reflects off everything in a 30-foot radius, including human bodies. Every movement—even the slightest ones, like breathing—causes a change in the reflected signal.

Katabi and her team developed machine-learning algorithms that analyze all these minute reflections. They trained the system to recognize simple motions like walking and falling, and more complex movements like those associated with sleep disturbances. “As you teach it more and more, the machine learns, and the next time it sees a pattern, even if it’s too complex for a human to abstract that pattern, the machine recognizes that pattern,” Katabi says.

Over time, the device creates large readouts of data that show patterns of behavior. The AI is designed to pick out deviations from those patterns that might signify things like agitation, depression, and sleep disturbances. It could also pick up whether a person is repeating certain behaviors during the day. These are all classic symptoms of Alzheimer’s.

“If you can catch these deviations early, you will be able to anticipate them and help manage them,” Vahia says.

In a patient with an Alzheimer’s diagnosis, Vahia and Katabi were able to tell that she was waking up at 2 a.m. and wandering around her room. They also noticed that she would pace more after certain family members visited. After confirming that behavior with a nurse, Vahia adjusted the patient’s dose of a drug used to prevent agitation.


Ipsit Vahia and Dina Katabi are testing an AI-powered device that Katabi’s lab built to monitor the behaviors of people with Alzheimer’s as well as those at risk of developing the disease.

Brain changes

AI is also finding use in helping physicians detect early signs of Alzheimer’s in the brain and understand how those physical changes unfold in different people. “When a radiologist reads a scan, it’s impossible to tell whether a person will progress to Alzheimer’s disease,” says Pedro Rosa-Neto, a neurologist at McGill University in Montreal.

Rosa-Neto and his colleague Sulantha Mathotaarachchi developed an algorithm that analyzed hundreds of positron-emission tomography (PET) scans from people who had been deemed at risk of developing Alzheimer’s. From medical records, the researchers knew which of these patients had gone on to develop the disease within two years of a scan, but they wanted to see if the AI system could identify them just by picking up patterns in the images.

Sure enough, the algorithm was able to spot patterns in clumps of amyloid—a protein often associated with the disease—in certain regions of the brain. Even trained radiologists would have had trouble noticing these issues on a brain scan. From the patterns, it was able to detect with 84 percent accuracy which patients ended up with Alzheimer’s.

Machine learning is also helping doctors predict the severity of the disease in different patients. Duke University physician and scientist P. Murali Doraiswamy is using machine learning to figure out what stage of the disease patients are in and whether their condition is likely to worsen.

“We’ve been seeing Alzheimer’s as a one-size-fits all problem,” says Doraiswamy. But people with Alzheimer’s don’t all experience the same symptoms, and some might get worse faster than others. Doctors have no idea which patients will remain stable for a while or which will quickly get sicker. “So we thought maybe the best way to solve this problem was to let a machine do it,” he says.

He worked with Dragan Gamberger, an artificial-intelligence expert at the Rudjer Boskovic Institute in Croatia, to develop a machine-learning algorithm that sorted through brain scans and medical records from 562 patients who had mild cognitive impairment at the beginning of a five-year period.

Two distinct groups emerged: those whose cognition declined significantly and those whose symptoms changed little or not at all over the five years. The system was able to pick up changes in the loss of brain tissue over time.

A third group was somewhere in the middle, between mild cognitive impairment and advanced Alzheimer’s. “We don’t know why these clusters exist yet,” Doraiswamy says.

Clinical trials

From 2002 to 2012, 99 percent of investigational Alzheimer’s drugs failed in clinical trials. One reason is that no one knows exactly what causes the disease. But another reason is that it is difficult to identify the patients most likely to benefit from specific drugs.

AI systems could help design better trials. “Once we have those people together with common genes, characteristics, and imaging scans, that’s going to make it much easier to test drugs,” says Marilyn Miller, who directs AI research in Alzheimer’s at the National Institute on Aging, part of the US National Institutes of Health.

Then, once patients are enrolled in a study, researchers could continuously monitor them to see if they’re benefiting from the medication.

“One of the biggest challenges in Alzheimer’s drug development is we haven’t had a good way of parsing out the right population to test the drug on,” says Vaibhav Narayan, a researcher on Johnson & Johnson’s neuroscience team.

He says machine-learning algorithms will greatly speed the process of recruiting patients for drug studies. And if AI can pick out which patients are most likely to get worse more quickly, it will be easier for investigators to tell if a drug is having any benefit.

That way, if doctors like Vahia notice signs of Alzheimer’s in a person like Graham, they can quickly get him signed up for a clinical trial in hopes of curbing the devastating effects that would otherwise come years later.

Miller thinks AI could be used to diagnose and predict Alzheimer’s in patients in as soon as five years from now. But she says it’ll require a lot of data to make sure the algorithms are accurate and reliable. Graham, for one, is doing his part to help out.

https://www.technologyreview.com/s/609236/ai-can-spot-signs-of-alzheimers-before-your-family-does/

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Longer duration of untreated psychosis was associated with accelerated hippocampal atrophy during initial antipsychotic treatment of first-episode schizophrenia, suggesting that psychosis may have persistent, negative effects on brain structure, according to finding published in JAMA Psychiatry.

“Several factors … have been linked to early psychosis and could mediate an association between [duration of untreated psychosis] and hippocampal volume loss, but evidence from longitudinal studies is lacking,” Donald C. Goff, MD, department of psychiatry, New York University Langone Medical Center, and colleagues wrote. “Whereas the negative association of [duration of untreated psychosis] with clinical course is attenuated by the initiation of antipsychotic treatment, the evidence is mixed as to whether antipsychotics contribute to loss of brain volume or protect against it.”

The extent to which loss of brain volume early in psychosis treatment reflects an illness effect, a drug effect or both remains unknown, according to the researchers. Therefore, Goff and colleagues examined loss of hippocampal volume during the first 8 weeks of treatment for schizophrenia, its link to duration of untreated psychosis and molecular biomarkers related to hippocampal volume loss and duration of untreated psychosis.

At Shanghai Mental Health Center in China, researchers conducted a longitudinal study with age- and sex-matched healthy controls between Mar. 5, 2013, and Oct. 8, 2014. They assessed 71 patients with nonaffective first-episode psychosis treated with second-generation antipsychotics and 73 controls. They reassessed 31 participants with psychosis and 32 controls 8 weeks later, measuring hippocampal volumetric integrity (HVI), duration of untreated psychosis, 13 molecular biomarkers and 14 single-nucleotide polymorphisms from 12 candidate genes.

Participants in the first-episode psychosis group had lower baseline median left HVI (n = 57) compared with those in the control group (n = 54; P = .001). Left HVI decreased in 24 participants with psychosis at a median annualized rate of –.03791 throughout the 8 weeks of treatment, whereas left HVI increased in 31 controls at a rate of 0.00115 (P = .001). Furthermore, researchers observed an inverse association between the change in left hippocampal volume and duration of untreated psychosis (P = .002).

Although they observed similar results in the right HVI, the relationship between change in right HVI and duration of psychosis was not significant. According to the results of analyses that looked at left-side hippocampal volume only, left HVI was associated with molecular biomarkers of inflammation, oxidative stress, brain-derived neurotrophic factor, glial injury and those reflecting dopaminergic and glutamatergic transmission.

“We found significantly lower HVI at baseline in participants with [first episode psychosis] compared with healthy controls and additional HVI reduction during antipsychotic treatment that correlated with [duration of untreated psychosis], consistent with a persistent, possibly deleterious, effect of untreated psychosis on brain structure,” Goff and colleagues wrote. “Larger longitudinal studies of longer duration are needed to examine the association between [duration of untreated psychosis], hippocampal volume and clinical outcomes.” – by Savannah Demko

https://www.healio.com/psychiatry/schizophrenia/news/online/%7Bf6c3c940-fe57-41d1-9eb7-7c835e3c48ea%7D/longer-duration-of-untreated-psychosis-linked-to-loss-of-brain-volume?utm_source=selligent&utm_medium=email&utm_campaign=psychiatry%20news&m_bt=1162769038120

After being stung by a parasitic wasp, the American cockroach loses control of its behavior, becoming host to the wasp’s egg. Days later, the hatchling consumes the cockroach alive. While this is a gruesome process for the cockroach, scientists now report in ACS’ journal Biochemistry the discovery of a new family of peptides in the wasp’s venom that could be key to controlling roach minds, and might even help researchers develop better Parkinson’s disease treatments.

Scientists have long studied venoms, such as that of the wasp, seeking out novel and potent molecules to treat disease, among other applications. In the case of the enigmatic wasp Ampulex compressa, it uses its venom in a two-pronged approach against the cockroach, with an initial sting to the thorax to paralyze the front legs and a subsequent sting directly to the brain. This second sting causes the roach first to vigorously groom itself, then to fall into a state of lethargy, allowing the wasp to do whatever it wants. This immobile state resembles symptoms of Parkinson’s disease, and both may be related to dysfunction in the dopamine pathway. In this study, Michael E. Adams and colleagues wanted to identify the ingredients in wasp venom that dictate this behavior.

The researchers milked wasps for their venom and then analyzed the components using liquid chromatography and mass spectrometry. They identified a new family of alpha-helical peptides and named them ampulexins. To test their function, the team injected the most abundant venom peptide into cockroaches. Afterward, the bugs needed, on average, a 13-volt electric shock to the foot to get them moving, while an average of 9 volts sufficed prior to the injection, suggesting the peptides help the wasp immobilize its prey. Future work will focus on identifying cellular targets of ampulexins, and potentially generating a useful animal model for the study of Parkinson’s disease treatments.

The authors acknowledge funding from the United States-Israel Binational Science Foundation, the University of California, Riverside Office of Research and Economic Development and the University of California Agricultural Experiment Station.

https://www.acs.org/content/acs/en/pressroom/presspacs/2018/acs-presspac-february-7-2018/mind-controlling-molecules-from-wasp-venom-could-someday-help-parkinsons-patients.html


Huntington’s neurons show multiple nuclei (blue) within the same cell, and other signs of trouble, long before symptoms emerge.

With new findings, scientists may be poised to break a long impasse in research on Huntington’s disease, a fatal hereditary disorder for which there is currently no treatment.

One in 10,000 Americans suffer from the disease, and most begin to show symptoms in middle age as they develop jerky movements—and as these patients increasingly lose brain neurons, they slide into dementia. But the new research suggests that these symptoms may be a late manifestation of a disease that originates much earlier, in the first steps of embryonic development.

A team at Rockefeller led by Ali Brivanlou, the Robert and Harriet Heilbrunn Professor, developed a system to model Huntington’s in human embryonic stem cells for the first time. In a report published in Development, they describe early abnormalities in the way Huntington’s neurons look, and how these cells form larger structures that had not previously been associated with the disease.

“Our research supports the idea that the first domino is pushed soon after fertilization,” Brivanlou says, “and that has consequences down the line. The final domino falls decades after birth, when the symptoms are observable.”

The findings have implications for how to best approach treating the disorder, and could ultimately lead to effective therapies.

A new tool

Huntington’s is one of the few diseases with a straightforward genetic culprit: One hundred percent of people with a mutated form of the Huntingtin (HTT) gene develop the disease. The mutation takes the form of extra DNA, and causes the gene to produce a longer-than-normal protein. The DNA itself appears in the form of a repeating sequence, and the more repeats there are, the earlier the disease sets in.

Research on Huntington’s has thus far relied heavily on animal models of the disease, and has left many key questions unanswered. For example, scientists have not been able to resolve what function the HTT gene serves normally, or how its mutation creates problems in the brain.

Suspecting that the disease works differently in humans, whose brains are much bigger and more complex than those of lab animals, Brivanlou, along with research associates Albert Ruzo and Gist Croft, developed a cell-based human system for their research. They used the gene editing technology CRISPR to engineer a series of human embryonic stem cell lines, which were identical apart from the number of DNA repeats that occurred at the ends of their HTT genes.

“We started seeing things that were completely unexpected,” says Brivanlou. “In cell lines with mutated HTT, we saw giant cells. It looked like a jungle of disorganization.”

When cells divide, they typically each retain one nuclei. However, some of these enlarged, mutated cells flaunted up to 12 nuclei—suggesting that neurogenesis, or the generation of new neurons, was affected. The disruption was directly proportional to how many repeats were present in the mutation: The more repeats there were, the more multinucleated neurons appeared.

“Our work adds to the evidence that there is an unrecognized developmental aspect to the pathology,” Brivanlou says. “Huntington’s may not be just a neurodegenerative disease, but also a neurodevelopmental disease.”

Toxic or essential?

Treatments for Huntington’s have typically focused on blocking the activity of the mutant HTT protein, the assumption being that the altered form of the protein was more active than normal, and therefore toxic to neurons. However, Brivanlou’s work shows that the brain disruption may actually be due to a lack of HTT protein activity.

To test its function, the researchers created cell lines that completely lacked the HTT protein. These cells turned out to be very similar to those with Huntington’s pathology, corroborating the idea that a lack of the protein—not an excess of it—is driving the disease.

The findings are significant, Brivanlou notes, since they indicate that existing treatments that were designed to block HTT activity may actually do more harm than good.

“We should rethink our approach to treating Huntington’s,” he says. “Both the role of the HTT protein and the timing of treatment need to be reconsidered; by the time a patient is displaying symptoms, it may be too late to medicate. We need to go back to the earliest events that trigger the chain reaction that ultimately results in disease so we can focus new therapies on the cause, not the consequences.”

The researchers hope their new cell lines will be a useful resource for studying the cellular and molecular intricacies of Huntington’s further, and suggest they may provide a model for examining other diseases of the brain that are specific to humans.

https://www.rockefeller.edu/news/21212-uncovering-early-origins-huntingtons-disease/


Prof Sarah Tabrizi , from the UCL Institute of Neurology, led the trials

By James Gallagher

The defect that causes the neurodegenerative disease Huntington’s has been corrected in patients for the first time, the BBC has learned. An experimental drug, injected into spinal fluid, safely lowered levels of toxic proteins in the brain. The research team, at University College London, say there is now hope the deadly disease can be stopped.

Experts say it could be the biggest breakthrough in neurodegenerative diseases for 50 years.

Huntington’s is one of the most devastating diseases. Some patients described it as Parkinson’s, Alzheimer’s and motor neurone disease rolled into one.

Peter Allen, 51, is in the early stages of Huntington’s and took part in the trial: “You end up in almost a vegetative state, it’s a horrible end.”

Huntington’s blights families. Peter has seen his mum Stephanie, uncle Keith and grandmother Olive die from it. Tests show his sister Sandy and brother Frank will develop the disease. The three siblings have eight children – all young adults, each of whom has a 50-50 chance of developing the disease.

The unstoppable death of brain cells in Huntington’s leaves patients in permanent decline, affecting their movement, behaviour, memory and ability to think clearly.

Peter, from Essex, told me: “It’s so difficult to have that degenerative thing in you.

“You know the last day was better than the next one’s going to be.”
Huntington’s generally affects people in their prime – in their 30s and 40s
Patients die around 10 to 20 years after symptoms start
About 8,500 people in the UK have Huntington’s and a further 25,000 will develop it when they are older

Huntington’s is caused by an error in a section of DNA called the huntingtin gene. Normally this contains the instructions for making a protein, called huntingtin, which is vital for brain development. But a genetic error corrupts the protein and turns it into a killer of brain cells.

The treatment is designed to silence the gene.

On the trial, 46 patients had the drug injected into the fluid that bathes the brain and spinal cord. The procedure was carried out at the Leonard Wolfson Experimental Neurology Centre at the National Hospital for Neurology and Neurosurgery in London. Doctors did not know what would happen. One fear was the injections could have caused fatal meningitis. But the first in-human trial showed the drug was safe, well tolerated by patients and crucially reduced the levels of huntingtin in the brain.

Prof Sarah Tabrizi, the lead researcher and director of the Huntington’s Disease Centre at UCL, told the BBC: “I’ve been seeing patients in clinic for nearly 20 years, I’ve seen many of my patients over that time die. For the first time we have the potential, we have the hope, of a therapy that one day may slow or prevent Huntington’s disease . This is of groundbreaking importance for patients and families.”

Doctors are not calling this a cure. They still need vital long-term data to show whether lowering levels of huntingtin will change the course of the disease. The animal research suggests it would. Some motor function even recovered in those experiments.

Peter, Sandy and Frank – as well as their partners Annie, Dermot and Hayley – have always promised their children they will not need to worry about Huntington’s as there will be a treatment in time for them. Peter told the BBC: “I’m the luckiest person in the world to be sitting here on the verge of having that. “Hopefully that will be made available to everybody, to my brothers and sisters and fundamentally my children.”

He, along with the other trial participants, can continue taking the drug as part of the next wave of trials. They will set out to show whether the disease can be slowed, and ultimately prevented, by treating Huntington’s disease carriers before they develop any symptoms.

Prof John Hardy, who was awarded the Breakthrough Prize for his work on Alzheimer’s, told the BBC: “I really think this is, potentially, the biggest breakthrough in neurodegenerative disease in the past 50 years. That sounds like hyperbole – in a year I might be embarrassed by saying that – but that’s how I feel at the moment.”

The UCL scientist, who was not involved in the research, says the same approach might be possible in other neurodegenerative diseases that feature the build-up of toxic proteins in the brain. The protein synuclein is implicated in Parkinson’s while amyloid and tau seem to have a role in dementias.

Off the back of this research, trials are planned using gene-silencing to lower the levels of tau.

Prof Giovanna Mallucci, who discovered the first chemical to prevent the death of brain tissue in any neurodegenerative disease, said the trial was a “tremendous step forward” for patients and there was now “real room for optimism”.

But Prof Mallucci, who is the associate director of UK Dementia Research Institute at the University of Cambridge, cautioned it was still a big leap to expect gene-silencing to work in other neurodegenerative diseases.

She told the BBC: “The case for these is not as clear-cut as for Huntington’s disease, they are more complex and less well understood. But the principle that a gene, any gene affecting disease progression and susceptibility, can be safely modified in this way in humans is very exciting and builds momentum and confidence in pursuing these avenues for potential treatments.”

The full details of the trial will be presented to scientists and published next year.

The therapy was developed by Ionis Pharmaceuticals, which said the drug had “substantially exceeded” expectations, and the licence has now been sold to Roche.

http://www.bbc.com/news/health-42308341

Last year, doctors of optometry detected more than 320,000 cases of diabetes. Imagine if they could make the same impact when it comes to exposing early signs of Alzheimer’s disease.

November is National Alzheimer’s Disease Awareness Month. An estimated 5.4 million Americans are affected by Alzheimer’s disease, according to the Centers for Disease Control and Prevention (CDC). Projections put the number at 13.8 million by 2050.

Maryke Nijhuis Neiberg, O.D., associate professor in the School of Optometry at Massachusetts College of Pharmacy and Heath Sciences, in Worcester, Massachusetts, considers this an unrealized patient education opportunity for doctors of optometry.

“The earlier diagnoses give doctors and patients a better chance at managing the progressive brain disease and preserving the patient’s quality of life,” Dr. Neiberg says. “There has been some increase in Alzheimer’s awareness over the years, particularly in the eye community, but not enough yet.

“Alzheimer’s is a significant future public health issue,” she adds. “It is still a terminal disease.”

Early intervention

Much of the research on Alzheimer’s disease seeks to slow the disease’s progression. For instance, a study in Biological Psychiatry on Nov. 6 by researchers at the University of Iowa and the University of Texas Southwestern Medical Center in Dallas reports that there may be a new treatment that can slow the depression and cognitive decline associated with Alzheimer’s disease, without affecting amyloid plaque deposits or reactive glia in rats.

Among the early signs of Alzheimer’s, the researchers say, are anxiety, depression and irritability-long before the devastating effects of memory loss.

“Thus, P7C3 compounds may form the basis for a new class of neuroprotective drugs for mitigating the symptoms in patients with Alzheimer’s disease by preserving neuronal cell survival, irrespective of other pathological events,” researchers say. “P7C3 compounds represent a novel route to treating depression, and new-onset depression in elderly patients may herald the development of Alzheimer’s disease with later cognitive impairments to follow.”

Another study in JAMA Ophthalmology in September by researchers at Stanford University and Veterans Affairs Palo Alto Health Care System linked visual impairment and cognition in older adults and also stressed the “potential importance” of vision screening in identifying these patients’ eye disease and cognitive deficits. The AOA strongly recommends comprehensive eye examinations and stresses the limitations of screenings.

Optometry’s role

According to the CDC:

The rate of Alzheimer’s jumped 50 percent between 1999 and 2014.

Americans fear losing their mental capacity more than losing their physical abilities.

More than $230 billion is estimated to be spent in 2017 on providing health care, long-term care, hospice plus unpaid care for relatives with Alzheimer’s and other dementias.

More large-scale research on Alzheimer’s needs to be done, but progress is being made. Dr. Neiberg pointed to research linking optical coherence tomography (OCT) of the macula to Alzheimer’s and Parkinson’s diseases.

“With the advent of OCT, we now know that the retinal ganglion cell layer thins and that the optic nerve cup-to-disc ratio increases in size, not unlike glaucoma,” Dr. Neiberg says. “Alzheimer’s produces visual field defects that are easily confused with glaucoma. What we need is large-scale research to determine how much of the normal tension glaucoma we diagnose and treat is ultimately related to Alzheimer’s disease.”

She adds, “The early perceptual changes that occur in early Alzheimer’s are startling and measurable. One of the earliest signs is a decline in the Benton Visual Retention Test, a test of visual memory. This test requires the duplication of shapes on paper with a pencil, and is scored.

“Research has shown that this test is able to predict high risk for Alzheimer’s 15 years before diagnosis,” she says. “It’s a simple test many developmental and pediatric optometrists already have on their shelves. If we combine that test and the ocular findings we see, we have a very strong indication that something is indeed amiss. Armed with this information, the patient can then consult with their primary care physician, initiate lifestyle modification and request a referral if necessary.”

There is no cure for Alzheimer’s disease. But doctors of optometry can engage patients in conversation about Alzheimer’s disease and how they can manage their own risk factors, including:

Smoking
Mid-life obesity
Sedentary lifestyle
High-cholesterol diet|
Vascular disease (i.e., diabetes and hypertension)

“Lifestyle modification and early access to medication, which can delay the progression of dementia, might be enough to keep the disease at bay for longer,” Dr. Neiberg says. “We should include the Alzheimer’s disease connection when we educate our patients about lifestyle diseases.”

https://finchannel.com/society/health-beauty/69483-doctors-of-optometry-can-spot-early-signs-of-alzheimer-s-disease

by CHRIS SMYTH

People living in areas with high levels of lithium in tap water are 17 per cent less likely to get dementia, according to a large study that suggests the naturally occurring metal could help to prevent mental decline.

The findings raise the possibility that lithium could one day be added to drinking water to protect the brain in the same way as fluoride is added to protect teeth.

Lithium is already widely available as a psychiatric drug and experts said the findings suggested that it could be used as a treatment to prevent dementia if further trials proved successful. Lithium is known to affect neurological signalling and has long been used as a treatment for conditions such as bipolar disorder. It occurs naturally in water and previous studies have found lower suicide rates in areas with higher levels.

Scientists studied 74,000 older people with dementia and 734,000 without across Denmark, comparing illness rates with lithium levels, which were 15 times higher in some areas.

Scientists at the University of Copenhagen found that dementia rates increased slightly with low levels of lithium before falling sharply above 10 micrograms per litre. At 15 to 27 micrograms/l, dementia rates were 17 per cent lower than for 2-5 micrograms/l, according to results published in JAMA Psychiatry.

The authors acknowledged that other factors could explain the results, including worse healthcare in the remoter areas that had less lithium in water, but they said it was plausible that tiny amounts in tap water could have a significant effect on dementia.

In a linked editorial John McGrath, of the University of Queensland, and Michael Berk, of the University of Melbourne, wrote: “In the spirit of alchemy, could we convert lithium, a simple metal used as a mood stabiliser, into a golden public health intervention that could prevent dementia?

They added: “That a relatively safe, simple, and cheap intervention (ie optimising lithium concentrations in the drinking water) could lead to the primary prevention of dementia is a tantalising prospect.”

David Smith, emeritus professor of pharmacology at the University of Oxford, said the findings tallied with MRI studies showing that lithium salts increased the volume of areas of the brain involved in Alzheimer’s. However, he added: “We should not be adding lithium salts to our tap water because we would not know what amount to use.”

David Reynolds, chief scientific officer at Alzheimer’s Research UK, said: “It is potentially exciting that low doses of a drug already available in the clinic could help limit the number of people who develop dementia.”

Rob Howard, professor of old-age psychiatry at University College London, said: “These results represent another important piece of evidence for lithium’s potential as a treatment for Alzheimer’s disease. We now need clinical trials of lithium in patients with Alzheimer’s disease to determine once and for all whether this cheap and well-tolerated element can slow dementia progression.”

http://www.theaustralian.com.au/news/world/the-times/lithium-in-tap-water-could-lower-dementia-risk/news-story/c40599203eca195402c03c0a168961a6