US Market News
3週前
TAO Synergies Set to Join the Russell Microcap® Index as a Leading Public Gateway to Decentralized AIJune 16, 2026 9:15 AM
PR Newswire (US) NEW YORK, June 16, 2026 /PRNewswire/ -- TAO Synergies Inc. (Nasdaq: TAOX) ("TAO Synergies" or the "Company"), the first pure play in capturing the opportunities emerging across decentralized artificial intelligence (DeAI) with its strategy centered on the Bittensor (TAO) ecosystem, a leading network powering decentralized AI, today announced its preliminary inclusion in the Russell Microcap® Index as part of the 2026 Russell Reconstitution.The Company's approach spans the full breadth of the Bittensor opportunity: owning TAO — where TAO Synergies is the largest publicly traded holder of TAO — as well as investing in Bittensor subnets, developing its own subnets, building decentralized AI applications, and pursuing additional opportunities across the DeAI landscape.The Russell Microcap® Index measures the performance of the microcap segment of the U.S. equity market and is widely used by investment managers and institutional investors for index funds and benchmarked investment strategies. Inclusion is expected to meaningfully increase TAO Synergies' visibility among institutional investors and the broader investment community, and to broaden the Company's exposure to index-oriented investment products."Joining the Russell Microcap® Index is a significant milestone that reflects TAO Synergies' growth and rising profile in the public markets," said Executive Chairman Joshua Silverman. "As one of the world's largest holders of TAO and a builder within the Bittensor ecosystem, we offer investors a differentiated, transparent way to participate in decentralized AI — one of the most compelling frontiers in technology today. We believe Russell Microcap Index inclusion will expand awareness of our strategy and bring it to a wider audience of institutional and index-oriented investors."The Russell Reconstitution is final after the close of the U.S. equity markets on Friday, June 26, 2026. Equity markets will open with the newly reconstituted Russell U.S. Indexes on Monday, June 29, 2026. Inclusion in the Russell Microcap® Index remains subject to FTSE Russell's final determination.About TAO SynergiesTAO Synergies Inc. (Nasdaq: TAOX) is the first pure-play public company dedicated to the intersection of cryptocurrency and artificial intelligence, focused on the opportunities emerging across decentralized AI and the Bittensor (TAO) ecosystem. The Company acquires and stakes TAO — ranking among the top 20 holders globally and as the largest publicly traded holder of TAO while investing in and developing Bittensor subnets, building decentralized AI applications, and pursuing further opportunities across the DeAI frontier. By providing transparent, regulated exposure to decentralized AI, TAO Synergies empowers investors to participate in the next era of technological disruption. For more information, visit www.taosynergies.com, taodaily.com, and @TAOSynergies on X.Forward-Looking StatementsAny statements contained in this press release that do not describe historical facts may constitute forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. Forward-looking statements generally can be identified by words such as "anticipates," "believes," "estimates," "expects," "intends," "plans," "projects," "will," and similar expressions. Such forward-looking statements are subject to risks and uncertainties and other influences, many of which the Company has no control over. These forward-looking statements include, among other things, statements about: the expected benefits of the Company's inclusion in the Russell Microcap® Index, including increased institutional visibility and broader exposure to index-oriented investment products; our decentralized AI strategy and our activities within the Bittensor ecosystem, including the acquisition and staking of TAO, investment in and development of subnets, and development of decentralized AI applications; our new media platform, including the accuracy of Bittensor-related information provided thereon; the reputational impact of our new media platform; the potential value to shareholders; and other factors described from time to time in documents that we file with the Securities and Exchange Commission. Actual results and the timing of certain events and circumstances may differ materially from those described by the forward-looking statements as a result of these risks and uncertainties, including, among other things, digital asset price volatility, regulatory changes affecting digital assets, and risks inherent in the Company's strategy. These and other factors are identified and described in more detail in the Company's filings with the Securities and Exchange Commission. Readers are cautioned not to place undue reliance on these forward-looking statements. The Company does not undertake to update these forward-looking statements.Investor Contact
800-811-5591
ir@taosynergies.com View original content:https://www.prnewswire.com/news-releases/tao-synergies-set-to-join-the-russell-microcap-index-as-a-leading-public-gateway-to-decentralized-ai-302801330.htmlSOURCE TAO Synergies Inc. Original: TAO Synergies Set to Join the Russell Microcap® Index as a Leading Public Gateway to Decentralized AI
Doc328
1年前
You are correct:
Cleveland Clinic
On February 23, 2022, the Company announced its collaboration with Cleveland Clinic to pursue possible treatments for Multiple Sclerosis (“MS”), and on July 19, 2023, the Company announced that it had entered into an agreement with Cleveland Clinic to conduct a Phase 1 trial of Bryostatin-1 in MS. Cleveland Clinic will manage the clinical trial’s implementation, including an IND submission to the FDA and patient enrollment. Cleveland Clinic has enrolled three subjects and has dosed two to - date, with the total planned enrollment in the MS Trial of 20 subjects. The total estimated costs associated with this collaboration are approximately $2.0 million. As of March 31, 2025, the Company has incurred expenses owed to Cleveland Clinic of approximately $528,000 of which $0 was expensed during the quarter ended March 31, 2025.
In December 2024, the Company announced via press release the termination of its agreement with the Cleveland Clinic due to the slow pace of enrollment in the Phase 1 clinical trial. The termination of the agreement was one of various actions authorized by the Board, designed to reduce cash burn rate.
HANUMAN
2年前
A study shows that rising levels of brain protein Aß42, not the reduction of amyloid plaques, better explains the cognitive benefits of new Alzheimer’s drugs. This finding challenges the traditional focus on plaques in Alzheimer’s treatment.
A new study reveals that the rise in protein levels due to new Alzheimer’s drugs may explain the slowing of cognitive decline just as effectively as the reduction of amyloid plaques.
In a study that questions the effectiveness of newly approved monoclonal antibodies in reducing cognitive decline in Alzheimer’s patients by clearing amyloid, researchers from the University of Cincinnati discovered that an unintended rise in a critical brain protein’s levels correlates just as strongly with cognitive benefits.
Led by UC’s Alberto Espay, MD, the research was published in the journal Brain.
Study background
For decades, the prevailing theory in the field has stated that a protein made up of 42 amino acids called amyloid-beta 42 (Aß42) hardens into clumps called amyloid plaques, and those plaques damage the brain, causing Alzheimer’s disease.
Espay and team have hypothesized that normal, soluble Aß42 in the brain is crucial for neuron health and that the loss of Aß42, rather than the buildup of plaques, drives Alzheimer’s. This includes published research that suggests dementia occurs not when plaque levels are high but when Aß42 levels drop very low.
According to Espay’s research, the transformation of Aß42 into plaques appears to be the brain’s normal response to biological, metabolic, or infectious stress.
Alberto Espay
Alberto Espay, MD, MSc, professor of neurology at the UC College of Medicine and Director and Endowed Chair of the James J. and Joan A. Gardner Family Center for Parkinson’s Disease and Movement Disorders. Credit: Colleen Kelley/UC Brand + Creative
“Most of us will accrue amyloid plaques in our brains as we age, and yet very few of us with plaques go on to develop dementia,” said Espay, professor of neurology in the UC College of Medicine and director and endowed chair of the James J. and Joan A. Gardner Family Center for Parkinson’s Disease and Movement Disorders at the UC Gardner Neuroscience Institute. “Yet the plaques remain the center of our attention in biomarker development and therapeutic strategies.”
Study details
Recently, several new monoclonal antibody medications designed to remove amyloid from the brain were approved after showing they lessened cognitive decline in clinical trials.
Espay and his colleagues noticed that these drugs unintentionally increased levels of Aß42.
“Amyloid plaques don’t cause Alzheimer’s, but if the brain makes too much of it while defending against infections, toxins, or biological changes, it can’t produce enough Aß42, causing its levels to drop below a critical threshold,” Espay explained. “That’s when dementia symptoms emerge.”
The team analyzed data from nearly 26,000 patients enrolled in 24 randomized clinical trials of these new antibody treatments, assessing cognitive impairment and differences in levels of Aß42 before and after treatment. They found that higher levels of Aß42 after treatment were independently associated with slower cognitive impairment and clinical decline.
“All stories have two sides — even the one we have told ourselves about how anti-amyloid treatments work: by lowering amyloid,” Espay said. “In fact, they also raise the levels of Aß42. Even if this is unintended, it is why there may be a benefit. Our study shows that we can predict changes in cognitive outcomes in anti-amyloid trials at least as well by the increases in Aß42 as by the decreases in amyloid.”
Espay said these findings fit well into his larger hypothesis about the root cause of Alzheimer’s, as increasing levels of Aß42 appear to improve cognition.
“If the problem with Alzheimer’s is the loss of the normal protein, then increasing it should be beneficial, and this study showed that it is,” he said. “The story makes sense: Increasing Aß42 levels to within the normal range is desirable.”
However, Espay believes these results also present a conundrum for clinicians because removing amyloid from the brain is toxic and may cause the brain to shrink faster after antibody treatment.
“Do we give patients an anti-protein treatment to increase their protein levels? I think the end, increasing Aß42, doesn’t justify the means, decreasing amyloid,” Espay said. Therapies that directly increase Aß42 levels without targeting amyloid are a focus of research for Espay and his group
Doc328
2年前
Here's a link to the trial on clinicaltrials.gov
https://clinicaltrials.gov/study/NCT06190912#participation-criteria
From inclusion criteria, it looks like this phase 1 will have a broad range of patients from no disability (EDSS 0) to using a walker (EDSS 7.0) and can have any form of MS (RRMS, SPMS, PPMS). This is open label with everyone receiving 14 doses over 26 weeks (similar dose as in the AD trials) and patients will continue on their existing MS medication. They can be on a stable dose of any MS med except teriflunomide (likely due to concerns of additive liver toxicity)
Cleveland clinic is one of the largest MS centers in the country and has access to a 7T research MRI, though all the MRI measures mentioned in the outcomes would be possible on a commercially available 3T (though not on 1.5T). However, Diffusion MRI and myelin water fraction will be more informative on a 7T. Though not on the list, I would expect them to also analyze paramagnetic rim lesions and grey matter lesion if the 7T is chosen.
If it is ever shown to have a benefit in MS, I suspect that bryostatin, based on MOA, would have more value in progressive MS than in earlier inflammatory/relapsing MS. With patients already on another DMT and with full range of disabilities in a small population for only 40 weeks, proving any clinical benefit will be very difficult in this study. Rather, I believe they are trying to prove a biologic effect and then will need to raise many millions to run a P2 for 2 years. From a science perspective this is very interesting but with a company having limited funds, the financial risk of investment is extremely high. A successful P1 trial still leads to a drug requiring many years of testing in a difficult indication
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