Omega-3s ‘could be vital in motor neurone disease and dementia protection'
A study led by the UK Dementia Research Institute and the UCL Institute of Healthy Ageing found the fats – which are found in oily fish, nuts and seeds – affect the conditions and may boost survival.
Previous studies have linked a high consumption of omega-3 fatty acids with a lower risk of developing MND and a longer lifespan for those with the condition.
However, until now, researchers have not understood why this occurs.
In the new research, experts increased the levels of healthy fats in the brain cells of fruit flies carrying a genetic mutation called C9orf72, while also examining human brain cells.
C9orf72 mutation is the most common genetic cause of MND and a rarer form of dementia known as frontotemporal dementia (FTD), which tends to affect younger people.
The team found that, at the start of the study, levels of poly-unsaturated fatty acids, including omega-3 fatty acids, were significantly reduced in the MND/FTD flies.
These fatty acids were also reduced in the brain cells of people with MND/FTD.
Experts specifically looked at alpha linoleic acid (ALA), a type of omega-3 fatty acid found in flaxseed, walnuts and soybean and vegetable oils such as canola oil.
They also looked at linoleic acid, a type of omega-6 fatty acid, found in similar foods.
Scientists fed the flies linoleic acid and alpha linoleic acid to test whether this would impact on their survival.
They found that increasing the amount of fatty acids in their diet led to a small improvement in the survival of the flies.
Next, they delivered the fatty acids directly to the brain cells of the flies which increased the survival of the flies by 83%, from 15 days to 27.5 days.
They repeated the experiment in cells taken from people with MND/FTD and found that increasing levels of the fatty acids in the cells prolonged survival.
The research, published in the journal Nature Neuroscience, was funded by Alzheimer's Research UK and the UK Dementia Research Institute.
Study leader Professor Adrian Isaacs, from the UK Dementia Research Institute, said: 'Epidemiological studies suggest that people with a high intake of omega-3 fatty acids have a lower risk of developing motor neuron disease.
'Our study adds a deeper understanding of the mechanisms behind this.
'From our findings we can conclude that enhancing levels of omega-3 fatty acids in the brain may be beneficial in motor neuron disease. Of course, the next step is to test this in people.
'We first need to work out which specific fatty acid would be best to test in humans, and how we can deliver sufficient quantities to the brain. Then, we want to take these findings forward into a clinical trial.'
The researchers also suggested the findings may also have implications for other neurodegenerative diseases.
Dr Julia Dudley, head of research at Alzheimer's Research UK, said: 'With nearly one million people living with dementia in the UK, there is an urgent need to understand and treat the diseases that cause this condition, including rarer forms.
'Neurodegenerative diseases are complex, however some share similar genetic changes.
'This means that understanding how these changes affect the brain could ultimately lead to new treatment approaches for dementia.
'It is exciting to see findings which suggest that increasing levels of fatty acids, including omega-3 could be protective against motor neuron disease and frontotemporal dementia.
'We are excited to see the next steps for this research which we hope will play a key role in bringing us closer to a cure.'
Last year, MND campaigner and Leeds Rhinos, Great Britain and England rugby league star Rob Burrow died from MND.
His family said they were inundated with messages of support when he died, including a 'heartfelt' message from the Prince of Wales.
MND, including its most common subtype amyotrophic lateral sclerosis (ALS), affects around one in 300 people in their lifetime and cannot be cured.
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Yahoo
6 days ago
- Yahoo
Alector Reports Second Quarter 2025 Financial Results and Provides Business Update
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As of June 30, 2025, Alector's cash, cash equivalents, and investments totaled $307.3 million. 'The topline results from the pivotal INFRONT-3 Phase 3 trial of latozinemab, expected by mid-fourth quarter, represent a key inflection point for Alector and for the FTD community,' said Arnon Rosenthal, Ph.D., Chief Executive Officer of Alector. 'FTD is a devastating form of dementia that affects people in the prime of life, has no approved treatments, and is often fatal within a decade of diagnosis. Heterozygous loss-of-function mutations in the GRN gene reduce progranulin levels by about 50%, impairing neuronal function and driving neurodegeneration. Latozinemab, our investigational therapy for FTD-GRN being developed in collaboration with GSK, is designed to restore progranulin levels in the brain. Supported by data from an open-label Phase 2 study, the FDA granted Breakthrough Therapy designation to latozinemab. The INFRONT-3 results will inform our next steps toward potential registration and may bring us one step closer to delivering a treatment for this relentless disease.' Dr. Rosenthal continued, 'In parallel, we are advancing AL101 in early Alzheimer's disease, with a placebo-controlled, double-blind, 76-week Phase 2 trial that is expected to complete in 2026. At the same time, we continue to build our preclinical and research pipeline, including brain-penetrant candidates enabled by our proprietary Alector Brain Carrier platform. Progressing late-stage clinical programs while investing in innovative early assets positions Alector to create near- and long-term value for both patients and shareholders. With a cash runway into the second half of 2027, we are well resourced to advance our scientific and strategic goals.' Sara Kenkare-Mitra, Ph.D., President and Head of Research and Development at Alector, added, 'Over the past quarter, we've made steady progress across our wholly owned preclinical and research pipeline, including programs powered by our proprietary Alector Brain Carrier platform. This technology is designed to deliver therapeutic cargos, including antibodies, proteins, enzymes, and siRNA, across the blood-brain barrier, a critical challenge in treating neurodegeneration. Using this approach, we're progressing brain-penetrant candidates, including our anti-amyloid beta antibody and anti-tau siRNA for Alzheimer's disease, as well as our engineered GCase enzyme replacement therapy for Parkinson's disease. This work underscores our commitment to developing first- and best-in-class therapies for patients with serious neurodegenerative diseases.' Recent Clinical Updates Latozinemab Alector and GSK remain on track to report topline data by the middle of the fourth quarter of 2025 from the pivotal, 96-week, randomized, double-blind, placebo-controlled INFRONT-3 Phase 3 trial evaluating latozinemab in frontotemporal dementia due to a GRN gene mutation (FTD-GRN). Pending the trial's outcome, the companies are preparing for potential Biologics License Application (BLA) and Marketing Authorization Application (MAA) submissions in 2026. The statistical analysis plan (SAP) for INFRONT-3 has been amended after engagement with the U.S. Food and Drug Administration (FDA). The SAP will include plasma progranulin (PGRN) as a co-primary endpoint along with the Clinical Dementia Rating® plus National Alzheimer's Coordinating Center Frontotemporal Lobar Degeneration Sum of Boxes (CDR® plus NACC FTLD-SB). Frontotemporal dementia (FTD) is a rare neurodegenerative disease and the most common form of dementia for people under the age of 60.1 It affects an estimated 50,000 to 60,000 individuals in the United States and roughly 110,000 in the European Union.2,3 There are several heritable forms of FTD, including FTD-GRN, which is caused by mutations in the GRN gene and represents about 5% to 10% of all cases.⁴ People with FTD often begin experiencing symptoms such as behavioral changes, lapses in judgment, and diminished language skills in their 40s and 50s.1 The disease typically progresses over 7 to 10 years and is ultimately fatal.5 Currently, there are no approved treatment options for any form of FTD.1 Heterozygous loss-of-function mutations in the GRN gene lead to haploinsufficiency, reducing PGRN levels in the central nervous system by 50%. These mutations are a known genetic cause of FTD.6 PGRN is a secreted glycoprotein that regulates lysosomal function, neuronal survival, and inflammation in the brain.6 Latozinemab is a novel, investigational human monoclonal antibody (mAb) designed to block and internalize the sortilin receptor to elevate PGRN levels in the brain. It is believed to be the most advanced therapeutic candidate in development for the treatment of FTD-GRN. Latozinemab has been granted Breakthrough Therapy and Fast Track designations by the FDA for the treatment of FTD-GRN, as well as Orphan Drug designation by both the FDA and the European Medicines Agency for the treatment of FTD. AL101/GSK4527226 The global, randomized, double-blind, placebo-controlled PROGRESS-AD Phase 2 clinical trial of AL101/GSK4527226 in early Alzheimer's disease (AD) is ongoing, with enrollment completed in April 2025 and trial completion expected in 2026. 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Preclinical and Research Pipeline Alector continues to advance its preclinical and early research pipeline, selectively supported by Alector Brain Carrier (ABC), the company's proprietary blood-brain barrier technology platform. The company is progressing ADP037-ABC, its brain-penetrant anti-amyloid beta antibody in AD; ADP050-ABC, its brain-penetrant engineered GCase enzyme replacement therapy in Parkinson's disease; and ADP064-ABC, its brain-penetrant anti-tau siRNA in AD, all of which are enabled by ABC. Alector is currently evaluating potential candidates and continues to target clinical entry for ADP037-ABC and ADP050-ABC in 2026, pending resource allocation, lead candidate selection, and the results of preclinical studies. Corporate News Neil Berkley, M.B.A., assumed the role of Interim Chief Financial Officer in June 2025 while continuing as Chief Business Officer. With a proven track record in corporate development and business strategy, Mr. Berkley brings insightful leadership to Alector as the company advances through key clinical and research milestones in his expanded role. In the third quarter of 2025, the U.S. Patent and Trademark Office issued a patent covering methods of treatment using latozinemab in individuals with FTD-GRN. Second Quarter 2025 Financial Results Revenue. Collaboration revenue for the quarter ended June 30, 2025, was $7.9 million, compared to $15.1 million for the same period in 2024. The $7.2 million decrease was mainly due to the satisfaction of the performance obligation associated with the AL002 program and the latozinemab FTD-C9orf72 Phase 2 trial in the fourth quarter of 2024. R&D Expenses. Total research and development expenses for the quarter ended June 30, 2025, were $27.6 million, compared to $46.3 million for the quarter ended June 30, 2024. The decrease of $18.7 million was mainly due to a decrease in research and development expenses for the AL002 program and latozinemab program as well as a decrease in personnel related costs as a result of the reductions in force. G&A Expenses. Total general and administrative expenses were $14.4 million for both the three months ended June 30, 2025, and the three months ended June 30, 2024. Net Loss. For the quarter ended June 30, 2025, Alector reported a net loss of $30.5 million, or $0.30 per share, compared to a net loss of $38.7 million, or $0.40 net loss per share, for the same period in 2024. Cash Position. Cash, cash equivalents, and investments were $307.3 million as of June 30, 2025. Management anticipates that this will be sufficient to fund Alector's operations into the second half of 2027. 2025 Guidance. Management is updating its guidance for the year ending 2025. The company anticipates collaboration revenue to be between $13 million and $18 million, total research and development expenses to be between $130 million and $140 million, and total general and administrative expenses to be between $55 million and $65 million. About AlectorAlector is a late-stage clinical biotechnology company focused on developing therapies to counteract the devastating progression of neurodegenerative diseases. Leveraging the principles of genetics, immunology, and neuroscience, the company is advancing a portfolio of genetically validated programs that aim to remove toxic proteins, replace missing proteins, and restore immune and nerve cell function. Supported by biomarkers, Alector's product candidates seek to treat a range of indications, such as frontotemporal dementia, Alzheimer's disease, and Parkinson's disease. The company is also developing Alector Brain Carrier (ABC), a proprietary blood-brain barrier platform, which is being selectively applied to its next-generation product candidates and research pipeline. ABC aims to enhance the delivery of therapeutics, achieve deeper brain penetration and efficacy at lower doses, and ultimately improve patient outcomes while reducing costs. Alector is headquartered in South San Francisco, California. For more information, please visit Forward-Looking StatementsThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Forward-looking statements in this press release include, but are not limited to, statements regarding our business plans, business strategy, product candidates, blood-brain barrier technology platform, research and preclinical pipeline, planned and ongoing preclinical studies and clinical trials, anticipated timing of and detail regarding release of data for INFRONT-3 and PROGRESS-AD, expected milestones, expectations of our collaborations, expectations of our interactions with regulatory authorities, and financial and cash guidance. Such statements are subject to numerous risks and uncertainties, including but not limited to risks and uncertainties as set forth in Alector's Quarterly Report on Form 10-Q filed on August 7, 2025, with the Securities and Exchange Commission ('SEC'), as well as the other documents Alector files from time to time with the SEC. These documents contain and identify important factors that could cause the actual results for Alector to differ materially from those contained in Alector's forward-looking statements. Any forward-looking statements contained in this press release speak only as of the date hereof, and Alector specifically disclaims any obligation to update any forward-looking statement, except as required by Consolidated Balance Sheet Data(in thousands) June 30, December 31, 2025 2024 Cash, cash equivalents, and marketable securities $ 307,280 $ 413,397 Total assets 356,422 468,303 Total current liabilities (excluding deferred revenue) 70,952 101,396 Deferred revenue (including current portion) 182,272 195,832 Total liabilities 285,247 341,503 Total stockholders' equity 71,175 126,800 Consolidated Statement of Operations Data(in thousands, except share and per share data) Three Months EndedJune 30, Six Months EndedJune 30, 2025 2024 2025 2024 Collaboration revenue $ 7,874 $ 15,083 $ 11,548 $ 30,976 Operating expenses: Research and development 27,611 46,314 61,252 91,481 General and administrative 14,401 14,375 29,129 28,809 Total operating expenses 42,012 60,689 90,381 120,290 Loss from operations (34,138 ) (45,606 ) (78,833 ) (89,314 ) Other income, net 3,614 7,003 7,838 14,639 Net loss before income tax (30,524 ) (38,603 ) (70,995 ) (74,675 ) Income tax expense — 73 — 80 Net loss $ (30,524 ) $ (38,676 ) $ (70,955 ) $ (74,755 ) Net loss per share, basic and diluted $ (0.30 ) $ (0.40 ) $ (0.71 ) $ (0.78 ) Shares used in computing net loss per share basic and diluted 100,371,632 96,674,921 99,887,605 95,242,548 REFERENCES The Association for Frontotemporal Degeneration (AFTD). Patient estimates based on internal forecasting analysis using published literature sources. E.U. estimates include EU5 countries only (Spain, Italy, France, U.K. and Germany). FTD Disorders Registry. Taylor R, Finger E. Frontotemporal dementias. Pract Neurol. 2019 Jun. Rhinn H, et al. Progranulin as a therapeutic target in neurodegenerative diseases. Trends Pharmacol Sci. 2022 Aug;43(8):641-652. Alector Contacts:AlectorKatie Hogan Argot Partners (media)David Rosen 646-461-6387alector@ Argot Partners (investors)Laura Perry 212-600-1902alector@
Yahoo
15-07-2025
- Yahoo
Right-to-Die Activist Ends Life by Starving Herself to ‘Protect My Children From Seeing Me Choke and Struggle to Breathe'
Two years ago, Emma Bray, 42, was diagnosed with a terminal neurological condition called motor neuron disease She decided to end her life by starving herself, hoping to spare her children from witnessing her decline any further The mom of two announced her own death on Instagram on July 14 alongside a final photo of herself lying in a hospice bedA British mother made the tough decision to starve herself to death to spare her children from witnessing the devastating effects of her terminal neurological condition. Two years ago, Emma Bray from Barnstaple, England, was diagnosed with motor neuron disease (MND). MND is a group of neurological disorders that gradually destroy the motor neurons, according to the Cleveland Clinic. These nerve cells are found in the brain and spinal cord, and they control muscle movement for activities like breathing, speaking, swallowing and walking. ALS — also known as Lou Gehrig's disease — is the most common MND. Never miss a story — sign up for to stay up-to-date on the best of what PEOPLE has to offer, from celebrity news to compelling human interest stories. 'I've had four different health professionals tell me I've got the worst disease possible,' she told The Mirror in May, using an eye-gazing machine to speak. 'I now feel I am at the stage where my quality of life is very affected, I can no longer use any of my limbs. My talking is severely affected, and I struggle to eat, and it's getting harder to breathe. I am only really comfortable in bed, and social visits are exhausting.' 'I have carers multiple times a day, can't be left alone overnight and can no longer do any basic tasks,' the 42-year-old continued. 'I can't scratch an itch, push up my glasses, or move a bed sheet if I am too hot or cold. I feel like I am losing the essence of me. I am still so loved, but I can't be myself, and I see that grief on everyone's faces." is now available in the Apple App Store! Download it now for the most binge-worthy celeb content, exclusive video clips, astrology updates and more! Bray — who actively campaigned for Dignity in Dying — was an advocate for the Assisted Dying Bill, which would allow adults in the UK who are terminally ill to have the choice of medical aid in dying. She said, if it were passed, it would've prevented her loved ones suffering for two years with anticipatory grief. 'Imagine seeing your children crying and upset and not be able to hug them or curl up in bed and wipe their tears away,' she told the outlet, referring to her children, age 15 and 14. 'This is hands down the thing I hate the most about motor neurone disease. It's taken my children's mum from them little by little.' So, Bray decided to end her life using the 'voluntarily stopping eating or drinking' practice, also known as VSED. According to nonprofit Compassion & Choices — which provides resources, training and support for those navigating end-of-life health care — VSED is 'when a mentally capable individual decides to control their own dying by making a conscious decision to refuse foods and fluids of any kind.' 'VSED is not an easy death, but with the current law in England, this is the only way I can have control over my death,' Bray explained. 'I want to protect my children from seeing me choke and struggle to breathe. I don't want to die, but I am going to and have come to terms with my impending death, and I know I want to die surrounded by loved ones, music and laughter, not in an emergency way after further decline.' 'My last bit of parenting I can do is to limit the suffering and trauma they have to witness,' she added. 'I made a promise to myself that I wanted to wait to see my daughter finish high school and my son grow up a little so I can picture the man he will become.' ! In her final months, she told the outlet that she's urging members of parliament to help others 'die with peace.' On Monday, July 14, Bray — from her @stupid_mnd account — posted on Instagram, announcing her own death alongside a final photo of herself lying in a hospice bed overlooking the trees. 'If you are reading this then I've finished my final spin round the sun,' she wrote. 'I've lived a very good life, surrounded by love, music and laughter and I want this to continue in my memory. Rather than shed a tear (or whilst you do) please plant a tree or call a friend, do a random act of kindness or take time to watch a sunset. For moments of doubt please ask 'what would Emma do?' and run with that probably inappropriate answer.' 'Hug everyone a little tighter and love openly,' she ended. 'Please surround those who were closest to me with love, time and patience. And to quote Frank Turner - Remember you get to dance another day but now you have to dance for one more of us. Love you , bye.' Read the original article on People
Yahoo
03-07-2025
- Yahoo
Dementia warning for rugby players as quarter show red flag signs
A new study suggests former rugby players show a higher prevalence of brain changes linked to dementia than matched members of the general population. Levels of a protein called p-tau217, a potential sign of dementia, were higher overall (17.6 per cent) in a group of 200 retired male and female players who said they had suffered significant previous head impact exposure in their careers, compared to 33 matched controls with no exposure to head injuries. Levels of the protein – common in people with diseases like Alzheimer's – were significantly increased in 46 (23 per cent) of the player group. MRI scans also revealed former players had reduced brain volume in some areas, compared with the control group. None of the participants were found to have dementia at the time of the study, which is ongoing and being conducted by researchers at Imperial College London, University College London and the UK Dementia Research Institute. Dr Jacqui Hanley, head of research at Alzheimer's Research UK, said: 'Although none of the rugby players developed young-onset dementia during the study, they did show changes known to be linked to dementia. READ MORE: Jessie J says she has chosen to stop taking some meds in cancer battle READ MORE: Foster care grandma killed trying to stop boy, 12, taking her car 'These include smaller brain volumes and higher levels of p-tau217 protein in the blood, which is common in people with diseases like Alzheimer's. It is too early to say whether these players will go on to develop dementia and whether the physical brain changes observed will predict cognitive difficulties later in their lives. 'There are also key limitations to bear in mind, such as the reliance on self-reporting and interview to determine traumatic brain injury history. However, as the study continues for another four years it should provide some insight into whether these markers in the blood and brain continue to change and how this could impact the rugby players' memory and thinking abilities.' Previous studies have suggested a link between playing rugby and football and an increased risk of developing neurodegenerative disease, such as the FIELD Study in football, which found footballers were three-and-a-half times more likely to die of neurodegenerative disease than age-matched members of the population. There are ongoing legal cases in rugby league, rugby union and football involving former players who claim the sporting authorities failed to adequately protect them from exposure to head injuries.
