Bill Gates reveals 'next phase of Alzheimer's fight' as he shares dad's personal battle
Bill Gates is speaking out about his personal experience with Alzheimer's — and his hope for progress in fighting the disease.
In an essay published this week on his blog at GatesNotes.com, the Microsoft co-founder and tech billionaire, 69, reflected on the difficulty of spending another Father's Day without his dad, Bill Gates Sr.
The elder Gates passed away in 2020 at the age of 94 after battling Alzheimer's.
"It was a brutal experience, watching my brilliant, loving father go downhill and disappear," Gates wrote in the blog post.
Today, motivated by his own experience with the common dementia, Gates — who serves as chair of the Gates Foundation — is committed to working toward a cure for the common dementia, which currently affects more than seven million Americans, or one in nine people over 65.
In his blog, Gates expressed optimism about the "massive progress" being made in the fight against Alzheimer's and other dementias.
Last year, Gates said he visited Indiana University's School of Medicine in Indianapolis to tour the labs where teams have been researching Alzheimer's biomarkers.
"I also got the opportunity to look under the hood of new automated machines that will soon be running diagnostics around the world," he wrote. "It's an exciting time in a challenging space."
One of the biggest breakthroughs in Alzheimer's research, according to Gates, is blood-based diagnostic tests, which detect the ratio of amyloid plaques in the brain. (Amyloid plaques, clumps of protein that accumulate in the brain, are one of the hallmarks of Alzheimer's.)
"I'm optimistic that these tests will be a game-changer," Gates wrote.
Last month, the U.S. Food and Drug Administration (FDA) approved the first blood-based test for patients 55 years and older, as Fox News Digital reported at the time.
"A simple, accurate and easy-to-run blood test might one day make routine screening possible."
Traditionally, Gates noted, the primary path to Alzheimer's diagnosis was either a PET scan (medical imaging) or spinal tap (lumbar puncture), which were usually only performed when symptoms emerged.
The hope is that blood-based tests could do a better job of catching the disease early, decline begins.
"We now know that the disease begins 15 to 20 years before you start to see any signs," Gates wrote.
"A simple, accurate and easy-to-run blood test might one day make routine screening possible, identifying patients long before they experience cognitive decline," he stated.
Gates said he is often asked, "What is the point of getting diagnosed if I can't do anything about it?"
To that end, he expressed his optimism for the future of Alzheimer's treatments, noting that two drugs — Lecanemab (Leqembi) and Donanemab (Kisunla) — have gained FDA approval.
"Both have proven to modestly slow down the progression of the disease, but what I'm really excited about is their potential when paired with an early diagnostic," Gates noted.
He said he is also hopeful that the blood tests will help speed up the process of enrolling patients in clinical trials for new Alzheimer's drugs.
To accomplish this, Gates is calling for increased funding for research, which often comes from federal grants.
"This is the moment to spend more money on research, not less," he wrote, also stating that "the quest to stop Alzheimer's has never had more momentum."
"There is still a huge amount of work to be done — like deepening our understanding of the disease's pathology and developing even better diagnostics," Gates went on.
"I am blown away by how much we have learned about Alzheimer's over the last couple of years."
Gates pointed out that when his father had Alzheimer's, it was considered a "death sentence," but that is starting to change.
"I am blown away by how much we have learned about Alzheimer's over the last couple of years," he wrote.
For more Health articles, visit www.foxnews.com/health
"I cannot help but be filled with a sense of hope when I think of all the progress being made on Alzheimer's, even with so many challenges happening around the world. We are closer than ever before to a world where no one has to watch someone they love suffer from this awful disease."
Hashtags
Try Our AI Features
Explore what Daily8 AI can do for you:
Comments
No comments yet...
Related Articles
Medscape
33 minutes ago
- Medscape
Fast Five Quiz: Alcohol Use Disorder
Alcohol use disorder remains a significant public health challenge in the United States, affecting more than 29 million individuals and contributing to more than 140,000 deaths each year. Despite its high prevalence and devastating health consequences, alcohol use disorder often goes underdiagnosed and undertreated. A widely accepted heuristic framework conceptualizes alcohol use disorder as a 3-stage cycle, binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation, offering clinicians a lens through which to understand its complex neurobiological underpinnings and diverse clinical presentations. Although effective behavioral therapies and several US Food and Drug Administration-approved medications are available for the treatment of alcohol use disorder, these interventions remain markedly underused, contributing to a substantial treatment gap. How much do you know about alcohol misuse and alcohol use disorder? Test your knowledge with this quick quiz. Alcohol misuse in alcohol use disorder can vary, from a pattern of intermittent episodes of binge drinking, to a pattern of prolonged heavy drinking over longer periods of time, to a continual drinking pattern due to fear of alcohol withdrawal. A heavy drinking day is defined as consuming 4 or more drinks for females and 5 or more drinks for males in a single day. In the United States, a standard drink is defined as 12 oz of beer, 5 oz of wine, and 1.5 oz of a distilled beverage. This definition helps identify patterns of alcohol misuse that might indicate alcohol use disorder. Learn more about alcoholism guidelines. Alcohol use disorder is more common in males, although the gap is narrowing. Although males are more likely to engage in frequent and heavy consumption, have a greater consumption of spirits, and experience higher rates of alcohol use mortality, females are at greater risk for certain health complications from alcohol, such as liver damage and experiencing higher blood alcohol concentrations at the same level of intake. Learn more about alcoholism presentation. The most frequent central nervous system consequence of persistent alcohol consumption is alcoholic cerebellar degeneration. This condition results from alcohol toxicity leading to damage of the cerebellum, the brain area responsible for coordination and balance. It commonly presents with gait instability, and balance problems, affecting 10%-25% of individuals with chronic alcohol use. Wernicke's encephalopathy is an acute, reversible condition caused by thiamine deficiency; it is not the most frequent long-term central nervous system consequence of alcohol consumption. Korsakoff syndrome is a chronic neuropsychiatric disorder that often follows untreated Wernicke's encephalopathy and is caused by malnutrition in combination with prolonged drinking. Although chronic alcohol use can lead to alcohol-related dementia, it occurs less frequently than alcoholic cerebellar degeneration. Learn more about Wernicke-Korsakoff syndrome. Alcoholic polyneuropathy, caused by prolonged alcohol use and often associated with nutritional deficiencies like thiamine deficiency, typically presents as a symmetrical sensory neuropathy. Females have a greater rate of alcoholic polyneuropathy. The most common symptoms of alcoholic polyneuropathy are ataxia, pain, and paresthesia. Other frequent symptoms include burning pain in the arms, soles of the feet and toes, and cramping in the calves and hands. Skin alterations do occur in alcoholic polyneuropathy, but they are considered secondary or less common symptoms compared with the hallmark neurological signs. The muscle weakness seen in alcoholic polyneuropathy primarily affects distal muscles, like the feet and hands. Hair loss can happen as a minor trophic change, but it is not a defining or common symptom of alcoholic polyneuropathy. Learn more about alcoholic neuropathy. Benzodiazepines are the recommended class of medication for treating alcohol withdrawal syndrome because they are effective in preventing severe complications of alcohol withdrawal syndrome, such as seizures and delirium tremens, and are considered the criterion standard treatment due to their fast onset, long duration, and safety profile. Selective serotonin reuptake inhibitors do not target the GABAergic or glutamatergic systems involved in alcohol withdrawal syndrome, making them ineffective for managing withdrawal symptoms. Beta-blockers can help control some autonomic symptoms like tremors or tachycardia but do not prevent seizures or delirium tremens, so they are not appropriate as primary treatment. N-methyl-D-aspartate receptor antagonists can modulate glutamate activity but lack enough evidence to be first-line therapy for alcohol withdrawal syndrome. Learn more about alcohol withdrawal syndrome.
Yahoo
38 minutes ago
- Yahoo
Late-night rocket launch in Florida: When to see from Vero Beach to Port St. Lucie to Fort Pierce
A late-night rocket launch from Florida is on the horizon. SpaceX is set to launch a batch of Starlink satellites into low-Earth orbit on June 22 from Cape Canaveral. Rockets here launch from NASA's Kennedy Space Center or nearby Cape Canaveral Space Force Station. Weather permitting and depending on cloud cover, a rocket launch from Florida's Space Coast could be visible as far north as Jacksonville Beach and Daytona Beach to as far south as Vero Beach and West Palm Beach. When there's a launch window in the middle of the night or very early morning, there's an opportunity for unique photos — the rocket lights up the dark sky and the contrail after makes for a great photo. Below is more information about the SpaceX rocket launch in Florida and suggestions on where to watch them from here. Rocket launch tally: Here's a list of all 2025 missions from Cape Canaveral, Florida (psst, there's a lot) For questions or comments, email FLORIDA TODAY Space Reporter Rick Neale at rneale@ or Space Reporter Brooke Edwards at bedwards@ For more space news from the USA TODAY Network, visit Tom Cruise and untitled SpaceX project: 'Mission: Impossible' star who lives in Florida may shoot a film in outer space Mission: A SpaceX Falcon 9 rocket will launch a payload of Starlink broadband satellites into low-Earth orbit, a National Geospatial-Intelligence Agency navigational warning shows. Launch window: 1:47 a.m. to 6:17 a.m. ET Sunday, June 22, 2025 Launch location: Launch complex 40 at Cape Canaveral Space Force Station in Cape Canaveral, Florida Sonic booms: No Trajectory: Northeast Live coverage starts 90 minutes before liftoff at : You can watch live rocket launch coverage from USA TODAY Network's Space Team, which consists of FLORIDA TODAY space reporters Rick Neale and Brooke Edwards and visuals journalists Craig Bailey, Malcolm Denemark and Tim Shortt. Our Space Team will provide up-to-the-minute updates in a mobile-friendly live blog, complete with a countdown clock, at starting 90 minutes before liftoff. You can download the free FLORIDA TODAY app, which is available in the App Store or Google Play, or type into your browser. Shown is the National Weather Service-Melbourne radar, which shows conditions in real-time for the Space Coast, Brevard County, Orlando and other parts of Florida. The current date and time show up on the bottom right of this radar embed; otherwise, you may need to clear your cache. Sebastian Inlet State Park, 9700 S. State Road A1A, Melbourne Beach, Florida (cost to enter) Wabasso Beach Park, 1808 Wabasso Beach Road, Wabasso, Florida Ambersands Beach Park, 12566 N. SR A1A, Vero Beach, Florida (free parking) South Beach Park, 1700 Ocean Drive, Vero Beach, Florida (free parking) Merrill Barber Bridge in Vero Beach, Florida Alma Lee Loy Bridge in Vero Beach, Florida Fort Pierce Inlet State Park, 905 Shorewinds Drive, Fort Pierce, Florida Blind Creek Beachside North and South, 5460 S. Ocean Drive, Fort Pierce, Florida Blue Heron Beach, 2101 Blue Heron Blvd., Fort Pierce, Florida Frederick Douglass Memorial Park, 3600 S. Ocean Drive, Fort Pierce, Florida Dollman Park Beachside, 9200 S. Ocean Drive, Jensen Beach, Florida Herman's Bay Beach, 7880 S. Ocean Drive, Jensen Beach, Florida John Brooks Park Beachside, 3300 S. Ocean Drive, Fort Pierce, Florida Middle Cove Beach, 4600 S. Ocean Drive, Fort Pierce, Florida Normandy Beach in Jensen Beach, Florida Pepper Park Beachside, 3302 N. SR A1A, Fort Pierce, Florida Walton Rocks Beach, 6700 S. Ocean Drive, Jensen Beach, Florida (dog park) Waveland Beach, 10350 S. Ocean Drive, Jensen Beach, Florida State Road A1A causeway in Stuart, Florida House of Refuge and beach, 301 S.E. MacArthur Blvd., Stuart, Florida This article originally appeared on Treasure Coast Newspapers: SpaceX nighttime rocket launch in Florida: What time is liftoff?
Yahoo
an hour ago
- Yahoo
OrsoBio to Present Preclinical Data on Mitochondrial Protonophore Portfolio in Models of Obesity at the American Diabetes Association's 85th Scientific Sessions
Data demonstrate the potential of TLC-6740 and TLC-1180 to induce weight loss while preserving lean mass, as monotherapy and in combination with an incretin, in obese mice MENLO PARK, Calif., June 20, 2025--(BUSINESS WIRE)--OrsoBio, Inc. ("OrsoBio" or "the Company"), a clinical-stage biopharmaceutical company developing treatments for obesity and obesity-associated disorders, today announced new preclinical data being presented at the 85th Scientific Sessions of the American Diabetes Association (ADA) being held June 20-23, 2025, in Chicago, Ill. The Company will present three abstracts highlighting the efficacy of its mitochondrial protonophores to induce weight loss and provide glycemic benefits while preserving lean mass in diet-induced obese (DIO) mice. The studies demonstrate the potential of TLC-6740 and TLC-1180—as monotherapy and in combination with the glucagon-like peptide-1 (GLP-1) receptor agonist semaglutide—for both the induction and maintenance of weight loss following incretin treatment. "The mechanism of our mitochondrial protonophores to increase energy expenditure complements that of incretins to enhance and sustain weight loss and provide additive metabolic benefits," said Mani Subramanian, MD, PhD, Chief Executive Officer of OrsoBio. "These preclinical findings mark an important step in fulfilling our mission to develop innovative, effective, oral therapies for obesity that preserve muscle and support cardiometabolic health." OrsoBio is advancing a pipeline of novel therapies targeting obesity through mechanistically distinct and complementary approaches. The Company's lead candidates include TLC-6740 and TLC-1180, both mitochondrial protonophores that promote weight loss by increasing energy expenditure. In addition, OrsoBio is developing TLC-3595, a selective inhibitor of acetyl-CoA carboxylase 2 (ACC2), designed to enhance fat oxidation. "GLP-1 receptor agonists have transformed obesity treatment but are limited by gastrointestinal side effects and loss of muscle mass," said Rob Myers, MD, Chief Medical Officer of OrsoBio. "Our preclinical data show that our mitochondrial protonophores drive sustained, fat-selective weight loss and metabolic benefits when combined with or sequenced after GLP-1 receptor agonists. These findings support our ongoing Phase 1b study of TLC-6740 in combination with tirzepatide (NCT05822544)." Poster information: Sequential Combination of the Mitochondrial Protonophore TLC-6740 With Semaglutide Normalizes Body Weight and Preserves Lean Mass in DIO MiceAbstract #1687-P Poster Session: Monday, June 23, 2025 (12:30 - 1:30 p.m. CT)This preclinical study assessed TLC-6740 alone, in combination with low-dose semaglutide (sequential combination), and as maintenance therapy following semaglutide discontinuation in DIO mice. The sequential combination of TLC-6740 with low-dose semaglutide produced superior body weight and fat mass loss, and improved glycemic parameters compared with TLC-6740 alone and high-dose semaglutide. Initiating TLC-6740 after semaglutide discontinuation maintained body weight and fat mass loss, and glycemic benefits. These findings support evaluation of TLC-6740 in combination with incretins in people living with obesity; a 24-week combination study of TLC-6740 with tirzepatide is ongoing (NCT05822544). De Novo or Sequential Combination of the Mitochondrial Protonophore TLC-1180 With Semaglutide Improves Weight Loss and Preserves Lean Mass in DIO MiceAbstract #1694-P Poster Session: Monday, June 23, 2025 (12:30 - 1:30 p.m. CT)This preclinical study evaluated the effects of TLC-1180 alone, in combination with semaglutide, and as a maintenance treatment following semaglutide discontinuation in DIO mice. As monotherapy, TLC-1180 demonstrated body weight and fat mass loss and preserved lean mass. Body weight and fat mass loss were amplified, and lean mass was preserved with TLC-1180 in combination with semaglutide. These benefits persisted when TLC-1180 was used as a maintenance treatment after semaglutide discontinuation. These data highlight the potential of TLC-1180 as monotherapy, in combination with incretins, or as maintenance therapy post incretin discontinuation in people living with obesity. Novel Combination of a Mitochondrial Protonophore and an Acetyl-CoA Carboxylase 2 (ACC2) Inhibitor Causes Weight Loss and Preserves Lean Mass in Obese MiceAbstract #1686-P Poster Session: Monday, June 23, 2025 (12:30 - 1:30 p.m. CT)This preclinical study evaluated the effects of the mitochondrial protonophore, TLC-1180, and the ACC2 inhibitor, TLC-3595—as monotherapy and in combination—and semaglutide in DIO mice. TLC-3595 dose dependently reduced body weight, fat mass, and liver biochemistry while preserving lean mass in DIO mice. A combination of TLC-3595 with TLC-1180 had similar weight loss efficacy to semaglutide, but preserved lean mass. Taken together, these data suggest that the novel, all-oral, non-incretin combination of TLC-3595 and TLC-1180 may cause similar weight loss to incretins and may afford additional advantages, including improved weight loss quality and/or tolerability (e.g., reduced incidence of gastrointestinal adverse events). About TLC-6740 TLC-6740 is a novel, oral, liver-targeted mitochondrial protonophore in development for the treatment of obesity and obesity-associated diseases, including diabetes and MASH. Based on active hepatic uptake and mitochondrial protonophore activity, TLC-6740 increases energy expenditure in hepatocytes, and is expected to have broad, systemic metabolic and cardiovascular benefits, including weight loss, improved insulin sensitivity, and as a treatment for MASH, and dyslipidemia. TLC-6740 is currently being evaluated in a Phase 1b clinical trial, as monotherapy and in combination with tirzepatide, in patients living with obesity (NCT05822544). About TLC-1180 TLC-1180 is a novel, potent, long-acting mitochondrial protonophore that has been shown to increase energy expenditure in mice with diet-induced obesity (DIO). In preclinical studies of DIO mice, TLC-1180 induced weight loss, improved glucose control, and enhanced the efficacy of GLP-1 receptor agonists, both as a single agent and in combination with incretins. TLC-1180 is currently completing IND-enabling studies and a first-in-human study is expected to initiate in 2025. About TLC-3595 TLC-3595 is a novel and selective ACC2 inhibitor designed to treat obesity and type 2 diabetes by increasing fatty acid oxidation (FAO), reducing ectopic lipid accumulation, and improving insulin sensitivity in skeletal muscle and liver. The compound may also have potential as a treatment for other conditions characterized by impaired FAO, including heart failure with preserved ejection fraction (HFpEF) and metabolic dysfunction-associated steatohepatitis (MASH). About OrsoBio, Inc. OrsoBio, Inc. is a privately held, clinical-stage biopharmaceutical company dedicated to developing therapies to treat obesity and obesity-associated disorders, including type 2 diabetes, MASH, and severe dyslipidemias. OrsoBio currently has four programs in clinical and preclinical development with first-in-class compounds that address central pathways in energy metabolism. For more information, please visit View source version on Contacts Media Contact Gwen GordonGwen@ Sign in to access your portfolio
