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Mizuho Upgrades Alector (ALEC) to Outperform, Raises PT to $3.50 on Q4 2025 Latozinemab Trial Anticipation
Mizuho Upgrades Alector (ALEC) to Outperform, Raises PT to $3.50 on Q4 2025 Latozinemab Trial Anticipation

Yahoo

timean hour ago

  • Business
  • Yahoo

Mizuho Upgrades Alector (ALEC) to Outperform, Raises PT to $3.50 on Q4 2025 Latozinemab Trial Anticipation

Alector Inc. (NASDAQ:ALEC) is one of the stocks under $10 to buy now. On July 28, Mizuho upgraded Alector from Neutral to Outperform, while raising the price target from $2.50 to $3.50. The decision reflected Mizuho's belief that the pessimism surrounding Alector's shares is excessive, especially considering the company's cash position of ~$350 million, which is roughly double its current valuation. Mizuho's confidence is also driven by feedback from key opinion leaders regarding latozinemab, which is Alector's lead asset for frontotemporal dementia/FTD, raising its probability of success from 50% to 60%. The firm favors the stock in anticipation of the Phase 3 data for latozinemab, expected in Q4 2025. The company is advancing its clinical pipeline, with the INFRONT-3 Phase 3 trial for latozinemab on schedule for topline data release in Q4 2025. A biotechnologist in a white lab coat manipulating genes in a laboratory. In Q1 2025, Alector reported revenue of $3.7 million, which fell short of the estimated $4.38 million. The revenue decline from $15.9 million in Q1 2024 was due to the completion of performance obligations related to the AL002 program and the latozinemab FTD-C9orf72 Phase 2 trial in late 2024. However, the net loss per share of $0.41 was better than the estimated loss of $0.48 per share. Alector Inc. (NASDAQ:ALEC) is a late-stage clinical biotechnology company that develops therapies that are focused on counteracting the devastating progression of neurodegenerative diseases. While we acknowledge the potential of ALEC as an investment, we believe certain AI stocks offer greater upside potential and carry less downside risk. If you're looking for an extremely undervalued AI stock that also stands to benefit significantly from Trump-era tariffs and the onshoring trend, see our free report on the . READ NEXT: and . Disclosure: None. This article is originally published at Insider Monkey. Error while retrieving data Sign in to access your portfolio Error while retrieving data

Alector to Host Second Quarter and Mid-Year 2025 Earnings Conference Call
Alector to Host Second Quarter and Mid-Year 2025 Earnings Conference Call

Yahoo

time8 hours ago

  • Business
  • Yahoo

Alector to Host Second Quarter and Mid-Year 2025 Earnings Conference Call

Call Scheduled for Thursday, August 7, 2025, at 4:30 p.m. ET/1:30 p.m. PT SOUTH SAN FRANCISCO, Calif., July 31, 2025 (GLOBE NEWSWIRE) -- Alector, Inc. (Nasdaq: ALEC), a late-stage clinical biotechnology company focused on developing therapies to counteract the devastating progression of neurodegeneration, today announced it will host a conference call and webcast on Thursday, August 7, 2025, at 4:30 p.m. ET to discuss results for the second quarter ended June 30, 2025, and provide a mid-year business update. The call will feature remarks from Ryan Darby, M.D., Associate Professor of Neurology and Director of the Frontotemporal Dementia Clinic at Vanderbilt University Medical Center, who will speak on the unmet need in frontotemporal dementia. A press release detailing second quarter results will be issued prior to the call. The event will be webcast live under the investor relations section of Alector's website at and following the event a replay will be archived there for 30 days. Interested parties participating by phone will need to register using this online form. After registering for dial-in details, all phone participants will receive an auto-generated e-mail containing a link to the dial-in number along with a personal PIN number to use to access the event by phone. 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 Alector Contacts: AlectorKatie Argot Partners (media)David Rosen646-461-6387alector@ Argot Partners (investors)Laura Perry212-600-1902alector@

Quanterix Launches Novel p-Tau 205 and p-Tau 212 Assays to Advance Alzheimer's Research at AAIC
Quanterix Launches Novel p-Tau 205 and p-Tau 212 Assays to Advance Alzheimer's Research at AAIC

National Post

time4 days ago

  • Business
  • National Post

Quanterix Launches Novel p-Tau 205 and p-Tau 212 Assays to Advance Alzheimer's Research at AAIC

Article content Company highlights expanded capabilities following Akoya Biosciences Acquisition and Simoa ® technology included in more than 55 posters and oral presentations at the annual conference demonstrating its impact on neurodegenerative disease research Article content BILLERICA, Mass. — Quanterix Corporation (NASDAQ: QTRX), a company fueling scientific discovery through ultrasensitive biomarker detection, today announced the first to market, commercial launch of two novel phospho-tau assays: p‑Tau 205 and p‑Tau 212, expanding its market-leading portfolio of blood-based biomarkers for Alzheimer's disease and neurodegeneration. The announcement comes alongside Quanterix's robust presence at the Alzheimer's Association International Conference (AAIC) 2025, with more than 55 posters and presentations featuring data generated using its Simoa ® technology. Article content These new assays enable the precise detection of tau phosphorylation sites, biomarkers increasingly associated with early and progressive stages of Alzheimer's disease. Developed on Quanterix's ultra-sensitive Simoa ® platform, our p‑Tau 205 and 212 assays empower researchers to explore novel disease mechanisms, refine patient stratification, and support therapeutic development through fluid-based biomarkers. Article content Quanterix's growing leadership in neurobiology was further reinforced by its recent acquisition of Akoya Biosciences, bringing advanced spatial proteomics into its scientific ecosystem. The Human FFPE Neurobiology Panel, originally developed by Akoya, complements the Simoa ® platform by enabling high-plex, spatially resolved analysis of disease-specific protein expression in brain tissue. Together, these platforms offer researchers a powerful combination of tissue- and fluid-based biomarker discovery to accelerate translation from bench to bedside. Article content 'The addition of p‑Tau 205 and 212 strengthens our ability to support the scientific community in its pursuit of earlier detection, deeper understanding, and more personalized treatment approaches for Alzheimer's,' said Masoud Toloue, PhD, CEO of Quanterix. 'Combined with the recent integration of Akoya's spatial biology platform, we are now uniquely positioned to offer researchers a multi-dimensional view of pathobiology—bridging the gap between soluble protein dynamics and spatial tissue context. By uniting two best-in-class technologies, we're advancing the future of precision diagnostics across neurology, oncology, and immunology.' Article content The newly launched p-Tau 205 and p-Tau 212 assays are now available to customers for use on the HD-X or SR-X instruments or testing directly through Quanterix's in-house Accelerator Lab, a CLIA-licensed, ISO 15189-accredited facility providing contract biomarker testing services to global partners in pharma, biotech, and academia. Article content To learn more about the new assays or Quanterix's expanded capabilities, visit or stop by the Quanterix booth at AAIC 2025. Article content About Quanterix Article content Quanterix is a global leader in ultra-sensitive biomarker detection, enabling breakthroughs in disease research, diagnostics, and drug development. Its proprietary Simoa ® technology delivers industry-leading sensitivity, allowing researchers to detect and quantify biomarkers in blood and other fluids at concentrations far below traditional limits. With more than 3,400 peer-reviewed publications, Quanterix has been a trusted partner to the scientific community for nearly two decades. In 2025, Quanterix acquired Akoya Biosciences, The Spatial Biology Company ®, adding multiplexed tissue imaging with single-cell resolution to its portfolio and 1,396 installed instruments. Together, the combined company offers a uniquely integrated platform that connects biology across blood and tissue—advancing precision medicine from discovery to diagnostics. Learn more at Article content Article content Article content Article content Contacts Article content Media Contact: Marissa Klaassen (781) 913.8036 media@ Article content

Stanford scientists 'totally surprised' by potential Parkinson's treatment discovery
Stanford scientists 'totally surprised' by potential Parkinson's treatment discovery

Fox News

time07-07-2025

  • Health
  • Fox News

Stanford scientists 'totally surprised' by potential Parkinson's treatment discovery

A recent study from Stanford Medicine that "totally surprised" researchers highlighted what could be a promising approach to slowing Parkinson's disease progression. The research, published in the journal Science Signaling, took a closer look at enzymes — proteins in the body that speed up chemical reactions and are essential for digestion, liver function and other key functions, according to Cleveland Clinic — and their role in Parkinson's. The team found that targeting a certain enzyme helped to restore neuron and cell communication in mice. Lead author Suzanne Pfeffer, PhD, the Emma Pfeiffer Merner Professor in Medical Sciences and a professor of biochemistry at Stanford, told Fox News Digital that the team was "totally surprised that we saw as much improvement as we did." In about 25% of Parkinson's cases, the culprit is some form of genetic mutation. One of the most common mutations creates an overactive enzyme called LRRK2, according to a Stanford press release. When there is too much LRRK2 activity, it changes the structure of the brain cells, disrupting important communication between neurons and cells. This system is crucial to movement, motivation and decision-making, according to the researchers. The goal of the study was to determine whether a specific molecule — the MLi-2 LRRK2 kinase inhibitor — could reverse the effect of overactive enzymes. Using mice that had the genetic mutation that causes overactive LRRK2 and also had symptoms consistent with early Parkinson's disease, the scientists tried feeding them the inhibitor for two weeks. There were initially no changes detected in brain structure, signaling or function of the dopamine neurons. However, after three months of eating the inhibitor, mice affected by the overactive enzyme appeared to have restored their neurons to the point where they were virtually the same as those without the genetic mutation, the study found. "Findings from this study suggest that inhibiting the LRRK2 enzyme could stabilize the progression of symptoms if patients can be identified early enough," Pfeffer said in the press release. The study did have some limitations, the researchers acknowledged. "This was in mice, not people, but our current results indicate that similar pathways are important in humans," Pfeffer told Fox News Digital. While the study focused on a specific genetic form of the disease, overactive LRRK2 is also present in other cases, meaning this treatment could help multiple types of Parkinson's patients and possibly those with other neurodegenerative diseases, the reseachers claimed. Looking ahead, the team plans to investigate whether other forms of Parkinson's could benefit. Parkinson's — a disease that involves the slow death of dopamine-producing neurons, leading to symptoms like tremors and stiffness — affects nearly one million Americans, according to the Parkinson's Foundation, which has offices in New York and Miami. Experts agree that early intervention is key, as Parkinson's symptoms often appear years after the disease begins. "These findings suggest that it might be possible to improve, not just stabilize, the condition of patients with Parkinson's disease." Identifying and treating at-risk individuals sooner could potentially halt or reverse neuron loss. "These findings suggest that it might be possible to improve, not just stabilize, the condition of patients with Parkinson's disease," Pfeffer said. For more Health articles, visit The researcher told Fox News Digital that it's important to encourage patients to undergo genetic testing to learn more about their suitability for clinical trials and future treatments. The study was funded by The Michael J. Fox Foundation for Parkinson's Research, the Aligning Science Across Parkinson's initiative and the United Kingdom Medical Research Council.

Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's

Yahoo

time06-07-2025

  • Health
  • Yahoo

Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's

Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight loss, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years

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