Category: Neurodegenerative Diseases

Categories : Neurodegenerative DiseasesTags :

CTE Is Caused by More Than Head Trauma, New Study Suggests

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Research reveals Alzheimer’s disease-like DNA damage, hints at immune involvement

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Chronic traumatic encephalopathy (CTE), a neurodegenerative disease diagnosed after death, most often athletes of contact sports and military personnel, is not just caused by repeated head impact but also linked to DNA damage similar to that seen in Alzheimer’s disease, according to a new study led by researchers at Harvard Medical School, Boston Children’s Hospital, Mass General Brigham, and Boston University.

CTE is known to share characteristics with Alzheimer’s disease, namely the buildup of abnormal tau protein in the brain. CTE has also been associated with the development of dementia. The new research, published October 30 in Science, highlights the commonalities between CTE and Alzheimer’s at the genetic level and raises hopes that future treatments could target both diseases.

The findings also support recent work from study co-authors Jonathan Cherry and Ann McKee at Boston University in suggesting that immune system responses could help explain why only some people with repeated head impact go on to develop CTE.

“Our results suggest that CTE develops through some process in addition to head trauma,” said co-senior author Christopher A. Walsh, Professor of Pediatrics and Neurology and chief of the Division of Genetics and Genomics at Boston Children’s. “We suspect it involves immune activation in a way similar to Alzheimer’s disease, happening years after trauma.”

A new approach to studying CTE

The team used two types of single-cell genomic sequencing to identify somatic genetic mutations – non-inherited changes in DNA. This marked the first time scientists took such an approach to studying CTE.

Studying postmortem brain tissue samples, the researchers analysed hundreds of neurons from the prefrontal cortex of 15 individuals diagnosed with CTE after death and 4 individuals with repeated head impact but without CTE and compared them with 19 neurotypical controls and 7 individuals with Alzheimer’s.

The team found that neurons from individuals with postmortem CTE diagnoses had specific abnormal patterns of somatic genome damage that closely resemble those seen in Alzheimer’s. Individuals displaying signs of repeated head impact without postmortem CTE diagnoses didn’t have these changes.

“One of the most significant aspects of our work is the introduction of a new, single-cell genome approach to CTE,” said co-senior author Michael Miller, HMS assistant professor of pathology at Brigham and Women’s Hospital. “Our study provides further evidence that CTE is a bona fide neurodegenerative disease defined by its unique neuropathological features.”

The researchers also observed that the CTE brain samples showed signs of damage equivalent to more than 100 years of excess aging.

Clues to CTE’s origins

Repeated head impact most often occurs during contact sports such as American football, hockey, and rugby or during military service. CTE has been found postmortem in the brains of teenagers and young adults playing amateur sports as well as in older professional athletes.

Recent research in Nature from Cherry and McKee found that repeated head impact causes brain damage in young people even before tau deposition or symptoms indicative of CTE arise. That study also indicated that repeated head trauma induces immune activation in athletes’ brains, said Walsh, who is also an investigator of the Howard Hughes Medical Institute.

The October 30 paper adds to this growing evidence base by linking CTE with Alzheimer’s, which involves inflammation in microglial cells in the brain, despite the diseases’ differing risk factors, Walsh said.

Source: Harvard Medical School

Categories : Neurodegenerative Diseases New Compounds and TreatmentsTags :

A New Treatment for Huntington’s Disease Is Genuinely Promising – But Here’s Why We Still Need Caution

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Photo by Anna Shvets

Bryce Vissel, UNSW Sydney

Imagine knowing in your 20s or 30s that you carry a gene which will cause your mind and body to slowly unravel. Huntington’s disease is inherited, relentless and fatal, and there is no cure. Families live with the certainty of decline stretching across generations.

Now, a new treatment is being widely reported as a breakthrough.

Last week, gene therapy company uniQure announced that a one-time brain infusion appeared to slow the disease in a small clinical study.

If confirmed, this would not only be a landmark for Huntington’s disease but potentially the first time a gene therapy has shown promise in any adult-onset neurodegenerative disorder.

But the results, which were announced in a press release, are early, unreviewed and based on external comparisons. So, while these findings offer families hope after decades of failure, we need to remain cautious.

What is Huntington’s disease?

Huntington’s is a rare but devastating disease, affecting around five to ten people in 100,000 in Western countries. That means thousands in Australia and hundreds of thousands worldwide.

Symptoms usually start in mid-life. They include involuntary movements, depression, irritability and progressive decline in thinking and memory. People lose the ability to work, manage money, live independently and eventually care for themselves. Most die ten to 20 years after onset.

The disease is caused by an expanded stretch of certain DNA repeats (CAG) in the huntingtin gene. The number of repeats strongly influences when symptoms begin, with longer expansions usually linked to earlier onset.

Looking for a treatment

The gene that causes Huntington’s disease was identified in 1993, 32 years ago. Soon afterwards, mouse studies showed that switching off the mutant huntingtin protein even after symptoms had begun could reverse signs and improve behaviour.

This suggested lowering the toxic protein might slow or even partly reverse the disease. Yet for three decades, every attempt to develop a therapy for people has failed to show convincing clinical benefit. Trials of huntingtin-lowering drugs and other approaches did not slow progression.

What is the new treatment?

The one-time gene therapy, called AMT-130, involves brain surgery guided by MRI. Surgeons infuse an engineered virus directly into the caudate and putamen brain regions, which are heavily affected in Huntington’s.

The virus carries a short genetic “microRNA” designed to reduce production of the affected huntingtin protein.

By delivering it straight into the brain, the treatment bypasses the blood–brain barrier. This natural wall usually prevents medicines from entering the central nervous system. That barrier helps explain why so many brain-targeted drugs have failed.

What did they find?

Some 29 patients received treatment, with 12 in each group (one low-dose, and one high-dose) followed for three years. According to uniQure, those given the higher dose declined much slower than expected.

The study compared how much participants’ movement, thinking and daily function declined, compared to a matched external group from a global Huntington’s registry (meaning they weren’t part of the study). The company claimed those given the higher dose had a 75% slowing in their decline.

On a functional scale focused on independence, the company reported a 60% slowing in decline for the higher dose group.

Other tests of movement and thinking also favoured treatment. Nerve-cell damage in spinal fluid was lower for study participants than would be expected for untreated patients.

Why should we be cautious?

These findings are an early snapshot of results reported by the company, not yet peer-reviewed. The study compared treated patients to an external matched control group, not people randomised to placebo at the same time. This design can introduce bias. The numbers are also small – only 12 patients at the three-year mark – so we can’t draw solid conclusions.

The company reports the therapy was generally well tolerated, with no new serious adverse events related to the drug since late 2022. Most problems were related to the neurosurgical infusion itself, and resolved. But in a disease that already causes such severe symptoms, it is often hard to know what counts as a side effect.

The company uniQure has said it plans to seek regulatory approval in 2026 on the basis of this dataset.

Regulators will face difficult decisions: whether to allow access sooner before all the questions and uncertainties are addressed – based on the needs of a community with no effective options – and wait for further data while people are being treated, or to insist on larger trials that confirm results before approval.

What does it mean?

If upheld, these results represent the first convincing signs that a gene-targeted therapy can slow Huntington’s disease. They may also be the first evidence of benefit from a gene therapy in any adult-onset neurodegenerative disorder. That would be a milestone after decades of failure.

But these results do not prove success. Only larger, longer and fully peer-reviewed studies will show whether this treatment truly changes lives. Even if approved, a complex neurosurgical gene therapy may not be easily accessible to all patients.

The company has said the drug’s price would be similar to other gene therapies – which can cost over A$3 million per patient – and will have the added cost of brain surgery.

The takeaway

For families who carry this gene, the hope is profound. But caution is just as important.

We may be witnessing the first credible step toward slowing an inherited adult-onset neurodegenerative disease, or just an early signal that may not hold up.

Ultimately, only time and rigorous science will show whether this treatment delivers the benefits so urgently needed.

Bryce Vissel, Cojoint Professor, School of Clinical Medicine, UNSW Sydney

This article is republished from The Conversation under a Creative Commons license. Read the original article.

Categories : Neurodegenerative DiseasesTags :

X-Chromosome Gene Behind Greater MS and Alzheimer’s Risk in Women

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Mouse study reveals how females’ double X chromosomes drives brain inflammation and identifies diabetes drug as potential treatment

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New research by UCLA Health has identified a sex-chromosome linked gene that drives inflammation in the female brain, offering insight into why women are disproportionately affected by conditions such as Alzheimer’s disease and multiple sclerosis as well as offering a potential target for intervention. 

The study, published in the journal Science Translational Medicine, used a mouse model of multiple sclerosis to identify a gene on the X chromosome that drives inflammation in brain immune cells, known as microglia. Because females have two X chromosomes, as opposed to only one in males, they get a “double dose” of inflammation, which plays a major role in ageing, Alzheimer’s disease and multiple sclerosis.  

When the gene, known as Kdm6a, and its associated protein were deactivated, the multiple sclerosis-like disease and neuropathology were both ameliorated with high significance in female mice.  

“It has long been known that there are sex differences in the brain. These can impact both health and neurological diseases,” said study lead author Dr Rhonda Voskuhl, director of the Multiple Sclerosis Program at UCLA Health and lead neurologist for the UCLA Comprehensive Menopause Program. “Multiple sclerosis and Alzheimer’s disease each affect women more often than men, about two to three times as often. Also, two-thirds of healthy women have ‘brain fog’ during menopause. These new findings explain why and point to a new treatment to target this.”  

When first author Dr Yuichiro Itoh of the Voskuhl lab genetically “knocked out” the gene Kdm6a in brain immune cells, the inflammatory molecules shifted from being activated to a resting state. Additionally, the Voskuhl team performed a pharmacologic “knock down” of the protein made by this gene using metformin. Metformin is widely used as a treatment for diabetes, but is currently being researched for potential anti-ageing properties.  

While these interventions were highly significant in female mice, their effect was almost undetectable in males, Voskuhl said. 

“This is consistent with there being ‘more to block’ in females due to having two copies of the X-linked gene,” said Voskuhl, who is also a professor of neurology at UCLA Health. “It’s also why females are more likely to get MS and AD than males. This has implications for the clinic. Women may respond differently to metformin treatment than men.” 

Voskuhl said the findings may also have implications for explaining a connection to brain fog in healthy women during menopause.  

“Sex chromosomes and sex hormones achieve a balance through evolution,” Voskuhl said. “There is a selection bias to do so. Females have a balance between X chromosome-driven inflammation that can be good to fight infections at child-bearing ages. This is held in check by oestrogen, which is anti-inflammatory and neuroprotective. As women age, menopause causes loss of oestrogen, unleashing the proinflammatory and neurodegenerative effects of this X chromosome the brain immune cell.”  

Voskuhl says together, these findings may support use of oestrogens that target the brain to keep the balance, and thereby protect the brain, during menopause.

Source: UCLA Health

Categories : Ageing Neurodegenerative DiseasesTags :

Is Physical Frailty a Cause of Dementia?

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A new study suggests that physical frailty may contribute to the development of dementia. The study was published on September 17, 2025, in Neurology®, the medical journal of the American Academy of Neurology.

Physical frailty is defined as having three or more of these five symptoms: often feeling tired; little or no physical activity; slow walking speed; low grip strength; and unintentional weight loss.

“We’ve known that frailty is associated with a higher risk of dementia, but our study provides evidence that frailty may be an actual cause of dementia,” said study author Yacong Bo, PhD, of Zhengzhou University in China. “On the other hand, despite this new evidence, we can’t rule out the possibility that frailty is instead a marker of the early changes in the disease process.”

The study involved 489 573 people with an average age of 57 who were followed for an average of 14 years. A total of 4.6% of the participants met the definition for frailty, with three or more of the symptoms. Another 43.9% who had one or two symptoms were categorised as pre-frailty and 51.5% had no symptoms and were categorised as not frail.

During the study, 8900 people developed dementia. A total of 4.6% of those with frailty developed dementia, compared to 2.2% of those with pre-frailty and 1.3% of those without frailty. After researchers adjusted for other factors that could affect the risk of dementia, such as age, education level and physical activity, they found that the people who met the definition for frailty were nearly three times more likely to develop dementia than those who had no symptoms of frailty.

Those categorised as pre-frailty were 50% more likely to develop dementia. People with frailty who also had genes linked to dementia were nearly four times more likely to develop dementia than those without frailty or the genetic risk. The researchers also analysed the data and found evidence suggesting that frailty may potentially be a factor in causing dementia.

“These findings reinforce the importance of identifying and managing frailty as a strategy for preventing dementia,” Bo said.

Looking at the data from the other direction, the researchers found that dementia is unlikely to increase the risk of frailty. The researchers also looked at brain imaging and biological biomarkers and found that people with frailty were more likely to have changes in their brain structure related to dementia.

“These biomarkers may be a mechanism underlying the pathway from frailty to dementia,” said Bo. A limitation of the study was that four of the five symptoms of frailty were reported by the participants, so they may not have provided accurate information.

Source: American Academy of Neurology

Categories : Neurodegenerative DiseasesTags :

Investigating Why Memory Circuits Break Down in Alzheimer’s Disease

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Scientists are investigating a small region of the brain that plays a major role in memory, spatial navigation, and perhaps Alzheimer’s disease. One of the first parts of the brain affected by Alzheimer’s disease is the entorhinal cortex – a region that plays a big role in memory, spatial navigation, and the brain’s internal mapping system.

With support announced in September from the Commonwealth of Virginia’s Alzheimer’s and Related Diseases Research Award Fund, Virginia Tech scientists Sharon Swanger and Shannon Farris are working to understand why this area is especially vulnerable.

Swanger studies how brain cells communicate across synapses, while Farris focuses on how memory at the molecular level. Their overlapping expertise made the collaboration a natural fit.

“We’ve both been studying for a while,” said Swanger, assistant professor at the Fralin Biomedical Research Institute at VTC. “This new collaborative project brings together my work on synapses and Shannon’s on mitochondria in a way that addresses a big gap in the field.”

“This kind of state-level support is critical,” said Farris, also an assistant professor at the research institute. “It gives researchers in Virginia the chance to ask questions that may eventually make a difference for people living with Alzheimer’s. It’s meaningful to be part of research that could help people facing that journey.”

A key focus of their research is mitochondria – tiny structures inside brain cells that provide the energy needed for a variety of cellular functions in neurons including transmission. In Alzheimer’s disease, mitochondria stop working properly early in the course of the disease.

Farris and Swanger are investigating whether mitochondria in a vulnerable memory-related circuit may become overloaded with calcium, a key signaling chemical for multiple neuronal and synaptic processes. That overload could contribute to the early breakdown of memory.

“The connection between these cells is one of the first to fail in Alzheimer’s,” Farris said. “We found that this synapse has unusually strong calcium signals in nearby mitochondria – so strong we can see them clearly under a light microscope. Those kinds of signals are hard to ignore. It gives us a model where we can really watch what’s happening as things start to go wrong.”

To test their hypothesis, the researchers will study brain tissue from healthy mice and mice with Alzheimer’s. By comparing how mitochondria function and how brain cells communicate across synapses in each group, they hope to find early signs of stress or failure in the entorhinal cortex–hippocampus circuit.

Source: Virginia Tech

Categories : Neurodegenerative DiseasesTags :

Breathing Low-oxygen Air Slows Parkinson’s Progression in Mice

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Researchers from the Broad Institute and Mass General Brigham have shown that a low-oxygen environment – similar to the thin air found at Mount Everest base camp – can protect the brain and restore movement in mice with Parkinson’s-like disease.

The new research, in Nature Neuroscience, suggests that cellular dysfunction in Parkinson’s leads to the accumulation of excess oxygen molecules in the brain, which then fuel neurodegeneration – and that reducing oxygen intake could help prevent or even reverse Parkinson’s symptoms.

“The fact that we actually saw some reversal of neurological damage is really exciting,” said co-senior author Vamsi Mootha, an institute member at the Broad, professor of systems biology and medicine at Harvard Medical School, a Howard Hughes Medical Institute investigator in the Department of Molecular Biology at Massachusetts General Hospital (MGH), a founding member of the Mass General Brigham healthcare system. “It tells us that there is a window during which some neurons are dysfunctional but not yet dead – and that we can restore their function if we intervene early enough.”

“The results raise the possibility of an entirely new paradigm for addressing Parkinson’s disease,” added co-senior author Fumito Ichinose, the William T. G. Morton professor of anesthesia at Harvard Medical School and MGH.

The researchers caution that it’s too soon to translate these results directly to new treatments for patients. They emphasize that unsupervised breathing of low-oxygen air, especially intermittently such as only at night, can be dangerous and may even worsen the disease. But they’re optimistic their findings could help spur the development of new drugs that mimic the effects of low oxygen.

The study builds on a decade of research from Mootha and others into hypoxia – the condition of having lower than normal oxygen levels in the body or tissues – and its unexpected ability to protect against mitochondrial disorders.

“We first saw that low oxygen could alleviate brain-related symptoms in some rare diseases where mitochondria are affected, such as Leigh syndrome and Friedreich’s ataxia,” said Mootha, who leads the Friedreich’s Ataxia Accelerator at Broad. “That raised the question: Could the same be true in more common neurodegenerative diseases like Parkinson’s?”

Eizo Marutani, an instructor of anesthesia at MGH and Harvard Medical School, is the first author of the new paper. 

A long-standing link

Parkinson’s disease, which affects more than 10 million people worldwide, causes the progressive loss of neurons in the brain, leading to tremors and slowed movements. Neurons affected by Parkinson’s also gradually accumulate toxic protein clumps called Lewy bodies. Some biochemical evidence has suggested that these clumps interfere with the function of mitochondria, that Mootha knew were altered in other diseases that could be treated with hypoxia.

Moreover, anecdotally, people with Parkinson’s seem to fare better at high altitudes. And long-term smokers – who have elevated levels of carbon monoxide, leading to less oxygen in tissues – also appear to have a lower risk of developing Parkinson’s.

“Based on this evidence, we became very interested in the effect of hypoxia on Parkinson’s disease,” said Ichinose.

Mootha and Ichinose turned to a well-established mouse model of Parkinson’s in which animals are injected with clumps of the α-synuclein proteins that seed the formation of Lewy bodies. The mice were then split into two groups: one breathing normal air (21% oxygen) and the other continuously housed in chambers with 11% oxygen – comparable to living at an altitude of about 4800m. 

A new paradigm for Parkinson’s

The results were striking. Three months after receiving α-synuclein protein injections, the mice breathing normal air had high levels of Lewy bodies, dead neurons, and severe movement problems. Mice that had breathed low-oxygen air from the start didn’t lose any neurons and showed no signs of movement problems, despite developing abundant Lewy bodies.

The findings show that hypoxia wasn’t stopping the formation of Lewy bodies but was protecting neurons from the damaging effects of these protein clumps – potentially suggesting a new mode of treating Parkinson’s without targeting α-synuclein or Lewy bodies, Ichinose said. 

What’s more, when hypoxia was introduced six weeks after the injection, when symptoms were already appearing, it still worked. The mice’s motor skills rebounded, their anxiety-like behaviors faded, and the loss of neurons in the brain stopped.

To further explore the underlying mechanism, the team analyzed brain cells of the mice and discovered that mice with Parkinson’s symptoms had much higher levels of oxygen in some parts of the brain than control mice and those that had breathed low-oxygen air. This excess oxygen, the researchers said, likely results from mitochondrial dysfunction. Damaged mitochondria can’t use oxygen efficiently, so it builds up to damaging levels. 

“Too much oxygen in the brain turns out to be toxic,” said Mootha. “By reducing the overall oxygen supply, we’re cutting off the fuel for that damage.”

Hypoxia in a pill

More work is needed before the findings can be directly used to treat Parkinson’s. In the meantime, Mootha and his team are developing “hypoxia in a pill” drugs that mimic the effects of low oxygen to potentially treat mitochondrial disorders, and they think a similar approach might work for some forms of neurodegeneration.

While not all neurodegenerative models respond to hypoxia, the approach has now shown success in mouse models of Parkinson’s, Leigh syndrome, Friedreich’s ataxia, and accelerated aging.

“It may not be a treatment for all types of neurodegeneration,” said Mootha, “but it’s a powerful concept – one that might shift how we think about treating some of these diseases.”

Source: Broad Institute

Categories : Neurodegenerative DiseasesTags :

Experiments Add to Evidence of Links Between Amyloid Deposits in Brain and Bone Marrow

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Neurons in the brain of an Alzheimer’s patient, with plaques caused by tau proteins. Credit: NIH

A recent study led by a team of researchers at The Johns Hopkins University School of Medicine examining aging mice has provided what is believed to be the first evidence that particles of amyloid beta protein, found in people with Alzheimer’s disease (AD), build up in the bone marrow of the animals, although not in the exact same form as the large, dense plaques found in the brains of people with Alzheimer’s disease.

“Although amyloid buildup has been found in organs outside the brain – such as the heart, kidneys, and nerves – it remains unclear whether similar deposits form in bone or bone marrow with aging or in Alzheimer’s disease,” says contributing study author Mei Wan, PhD, professor of the department of Orthopaedic Surgery. While brain amyloid has been extensively studied for its role in memory loss and neurodegeneration, far less is known about amyloid elsewhere in the body. In fact, almost nothing is known about whether amyloid forms in the skeleton or how it might contribute to age-related bone loss.”

AD is primarily associated with excessive amyloid plaques in the brain. Osteoporosis is a bone disease marked by low bone mineral density with an increased risk of fractures. Recent research suggests these two age-related conditions may be connected, and scientists are beginning to uncover common underlying causes.

Funded by the National Institutes of Health, the study findings, published in Nature Aging, advance scientific understanding of long-suspected similar biological processes that may be at work in osteoporosis – a form of bone loss – and Alzheimer’s dementia, the researchers say. The work may also offer potential new targets for preventing or treating bone loss.  

The buildup of amyloid is triggered by fat cells in the bone marrow, known as bone marrow adipocytes (BMAds), and a protein they release called SAP/PTX2 in aged mice and mice with AD. These amyloid deposits impair bone-building cells (osteoblasts) and activate bone-resorbing cells (osteoclasts), leading to bone loss. In previous mouse models, removing senescent BMAds or blocking SAP/PTX2 have shown to significantly reduce amyloid buildup and restored bone health.

In this study, male and female mice ranging from 4 to 24 months were kept in a temperature-controlled room provided with ongoing access to food and water and exposed to a 12-hour light-dark cycle. Researchers put a concentration of 5mg/ml in the drinking water of the mice aged 18 months and examined the effects CPHPC had on their age-related bone loss. CPHPC (also named Miridesap) is a small molecule compound originally designed to treat amyloidosis which is a rare disease marked by the buildup of amyloid proteins. A control group of mice aged 4, 9, 22 and 24 months were given the same dosage of water without the CPHPC drug  

High-resolution imaging of thigh and shin bones revealed amyloid fibrils forming ring-like structures around BMAds in aged mice and mice genetically engineered to have a form of AD. SAP/PTX2-driven amyloid clumps were found to enhance bone loss.

Study results also showed that CPHPC successfully depleted SAP/PTX2 and reversed bone deterioration in the older mice, suggesting a promising new therapeutic strategy for osteoporosis in the elderly, a strategy that would seek to eliminate aging fat cells or amyloid-promoting proteins.  

Wan adds, “Our study is what we believe to be the first to show that harmful amyloid fibres (Aβ fibrils) build up in the bone marrow of aged mice. We also found that fat cells in the bone marrow release a protein called SAP/PTX2, which plays a major role in triggering this amyloid buildup and damaging bone. These findings uncover a new connection between bone loss and dementia risk and may open the door to new research on how protecting bone health could also help protect brain function.”

This discovery provides an opportunity for new treatments targeting bone aging and Alzheimer’s-associated osteoporosis by focusing on the elimination of senescent fat cells or amyloid-promoting proteins.

Source: Johns Hopkins Medicine

Categories : Diet and Nutrition Neurodegenerative DiseasesTags :

Significant Drop in Omega Fatty Acids in Women with Alzheimer’s

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Analysis of lipid blood levels in women with Alzheimer’s disease has shown noticeable loss of unsaturated fats, such as those that contain omega fatty acids, compared to healthy women.

In men with Alzheimer’s, no significant difference was found in the same lipid molecule composition disease compared to healthy men, which suggests that those lipids have a different role in the disease according to sex. Fats perform important roles in maintaining a healthy brain, so this study could indicate why more women are diagnosed with the disease.

The study, published today in Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association by scientists from King’s College London and Queen Mary University London, is the first to reveal the important role lipids could have in the risk for Alzheimer’s between the sexes.

Women are disproportionately impacted by Alzheimer’s Disease and are more often diagnosed with the disease than men after the age of 80. One of the most surprising things we saw when looking at the different sexes was that there was no difference in these lipids in healthy and cognitively impaired men, but for women this picture was completely different. The study reveals that Alzheimer’s lipid biology is different between the sexes, opening new avenues for research.

Dr Cristina Legido-Quigley, Reader in Systems Medicine

The scientists took plasma samples from 841 participants who had Alzheimer’s Disease, mild cognitive impairment and cognitively health controls and and were measured for brain inflammation and damage.

They used mass spectrometry to analyse the 700 individual lipids in the blood. Lipids are a group of many molecules. Saturated lipids are generally considered as ‘unhealthy’ or ‘bad’ lipids, while unsaturated lipid, which sometime contains omega fatty acids, are generally considered ‘healthy’.

Scientists saw a steep increase in lipids with saturation – the ‘unhealthy lipids’ – in women with Alzheimer’s compared to the healthy group. The lipids with attached omega fatty acids were the most decreased in the Alzheimer’s group.

Now, the scientists say there is a statistical indication that there is a causal link between Alzheimer’s Disease and fatty acids. But a clinical trial is necessary to confirm the link.

Dr Legido-Quigley added: “Our study suggests that women should make sure they are getting omega fatty acids in their diet – through fatty fish or via supplements. However, we need clinical trials to determine if shifting the lipid composition can influence the biological trajectory of Alzheimer’s Disease.”

Dr Asger Wretlind, first author of the study from the School of Cancer & Pharmaceutical Sciences, said: “Scientists have known for some time that more women than men are diagnosed with Alzheimer’s disease. 

Although this still warrants further research, we were able to detect biological differences in lipids between the sexes in a large cohort, and show the importance of lipids containing omegas in the blood, which has not been done before. The results are very striking and now we are looking at how early in life this change occurs in women.

Dr Asger Wretlind, School of Cancer & Pharmaceutical Sciences

Source: King’s College London

Categories : Metabolic Disorders Neurodegenerative DiseasesTags :

Does Metformin Possibly Help Prevent Dementia?

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New research in Diabetes, Obesity and Metabolism reveals that metformin, a medication traditionally prescribed to treat diabetes, is linked to lower risks of dementia and early death.

In the study by investigators at Taipei Medical University that included 452,777 adults with varying degrees of overweight and obesity, 35,784 cases of dementia and 76,048 deaths occurred over 10 years. Metformin users exhibited significantly lower risks of both dementia and all-cause death than nonusers.

The benefits of metformin were seen across all categories of overweight, obesity, and severe obesity, with 8–12% lower risks of dementia and 26–28% lower risks of death.

“Although our study results are promising for metformin’s effects on dementia and mortality, further research is required to explore the mechanisms involved,” said co-corresponding author Chiehfeng Chen, MD, PhD, MPH.

Source: Wiley

Categories : Neurodegenerative DiseasesTags :

Bio Detection Dogs Successfully Detect Parkinson’s Disease by Odour

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People with Parkinson’s disease (PD) have an odour that can be reliably detected from skin swabs by trained dogs, a new study shows. The research, in collaboration with Medical Detection Dogs and the Universities of Bristol and Manchester, is published in The Journal of Parkinson’s Disease.

Two dogs were trained by the charity, Medical Detection Dogs, to distinguish between sebum swabs from people with and without Parkinson’s disease.

In a double blind trial, they showed sensitivity of up to 80% and specificity of up to 98%.

Not only that, they detected it in samples from patients who also had other health conditions.

The dogs were trained over a number of weeks on over 200 odour samples from individuals that had tested positive for PD and control samples from people who did not have the disease. Samples were presented to the dogs on a stand system and the dogs were rewarded for correctly indicating a positive sample and for correctly ignoring a negative sample.

In the double-blind testing, meaning that only a computer knew where the correct samples were, each line was also presented in reverse order so that samples for which no decision was made were re-presented. Then any unsearched samples were collected together in new lines, until a decision had been made for all samples.

A definitive diagnostic test for Parkinson’s Disease (PD) remains elusive, so identification of potential biomarkers could help diagnosis and timely intervention.

Claire Guest, Medical Detection Dogs CEO and Chief Scientific Officer, says: “We are extremely proud to say that once again, dogs can very accurately detect disease.

“There is currently no early test for Parkinson’s disease and symptoms may start up to 20 years before they become visible and persistent leading to a confirmed diagnosis.

“Timely diagnosis is key as subsequent treatment could slow down the progression of the disease and reduce the intensity of symptoms.”

Nicola Rooney, Associate Professor at Bristol Veterinary School at the University of Bristol and lead author, says: “Identifying diagnostic biomarkers of PD, particularly those that may predict development or help diagnose disease earlier is the subject of much ongoing research. The dogs in this study achieved high sensitivity and specificity and showed there is an olfactory signature distinct to patients with the disease. Sensitivity levels of 70% and 80% are well above chance and I believe that dogs could help us to develop a quick non-invasive and cost-effective method to identify patients with Parkinson’s disease.”

Perdita Barran, Professor of Mass Spectrometry at The University of Manchester, said: “It’s wonderful to be part of this research inspired by Joy Milne and our Nose2Diagnose programme. This study adds to the growing body of evidence showing that simple, non-invasive skin swabs can be used to diagnose Parkinson’s disease, offering a faster and more accessible method for early detection.”

The two dogs in the study were Golden Retriever, Bumper and Black Labrador, Peanut.

Source: University of Bristol