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Meta Just Achieved Mind Reading with AI: A Breakthrough in Brain-Computer Interface Technology

Meta, the parent company of Facebook, has made a groundbreaking development in brain-computer interface technology. They have unveiled an AI system that can decode visual representations and even “hear” what someone is hearing by studying their brainwaves. These advancements in brain-machine interface technology have the potential to transform our relationship with artificial intelligence and its potential applications in healthcare, communication, and virtual reality.

The University of Texas at Austin has developed a new technology that can translate brain activity into written text without surgical implants. This breakthrough uses functional Magnetic Resonance Imaging (fMRI) scan data to reconstruct speech. An AI-based decoder then creates text based on the patterns of neuronal activity that correspond to the intended meaning. This new technology could help people who have lost the ability to speak due to conditions such as stroke or motor neuron disease.

Despite the fMRI having a time lag, which makes tracking brain activity in real-time challenging, the decoder was still able to achieve impressive accuracy. The University of Texas researchers faced challenges in dealing with the inherent “noisiness” of brain signals picked up by sensors, but by employing advanced technology and machine learning, they successfully aligned representations of speech and brain activity. The decoder works at the level of ideas and semantics, providing the gist of thoughts rather than an exact word-for-word translation. This study marks a significant advance in non-invasive brain decoding, showcasing the potential for future applications in neuroscience and communication.

Brain implant may enable communication from thoughts alone

A speech prosthetic developed by a collaborative team of Duke neuroscientists, neurosurgeons, and engineers can translate a person’s brain signals into what they’re trying to say.

  • A pioneering speech prosthetic translates brain signals into speech, aiming to assist those with speech-affecting neurological disorders.
  • The device employs a high-density sensor array to capture brain activity with unprecedented detail.
  • Site-specific encoding of photoactivity and photoreactivity into antibody fragments

    New light activated cancer treatment.


    Several antibodies and antibody fragments have been previously developed for the treatment of various diseases, including cancer3,4. These antibodies bind to cell surface receptors expressed at higher levels on cancer cells, addressing a major challenge of selective cell targeting in cancer therapy. Although full-length antibodies have shown promise for treatment of several cancers, limited success has been demonstrated in eliminating solid tumors. Due to their large size, full-length antibodies are unable to diffuse deep into solid tumors5. In addition, it has been shown that high-affinity antibodies bind to the periphery of the tumor tissues, forming a barrier and preventing their further penetration6. Some studies in patients with cancer estimate that only 0.01% of the injected antibodies accumulate per gram of solid tumor tissue7. Small antibody fragments with low molecular weight can diffuse much deeper into tissues, presenting an excellent alternative to full-length antibodies. However, small antibody fragments have a low residence time in the body and often have a higher rate of dissociation (koff) from the target compared with full-length antibodies, limiting their clinical utility8. To address these challenges, antibody fragments are often multimerized9,10 and/or conjugated to larger proteins11, which increases the size of antibody fragments, again reducing their ability to penetrate into the tumor.

    One solution to overcome the limitation of low residence time would be to replace the noncovalent interactions between the antibody fragment and its antigen with a covalent bond. In a notable effort, an affibody containing a photocrosslinker in its antigen binding region was shown to covalently link to its antigen and demonstrated higher accumulation on tumor tissues12. Another pioneering study involved developing affibodies containing a latent bioreactive amino acid in their antigen binding region that forms a covalent bond with the target antigen by proximity-dependent reaction without any external impetus13. However, the former had substantially lower binding affinity compared with its wild-type (wt) counterpart and thus, requires using a high concentration for efficient initial binding, while the latter could react with target antigen expressed on healthy cells causing side effects.

    Although antibody-based therapeutics are more selective than several cytotoxic small molecule drugs used for cancer treatment, they can cause cardiac toxicity and skin reactions14. These side effects are due to the binding of the antibody to its receptor antigen expressed on healthy cells. This challenge could be addressed by activating antibody–antigen binding in the tumor microenvironment. One notable example in this direction is the development of antibodies containing an inhibitory N-terminal domain that is removed by tumor-specific proteases15. However, this approach would be difficult to extend to antibody fragments whose N terminus is not involved in antigen binding. We and others have also developed light-activated antibody fragments either by site-specific installation of photocaged functional groups or by introducing light-responsive proteins into antibodies16,17,18. In principle, such antibodies could be activated at the site of tumors using surgically implanted biocompatible light-emitting diodes (LEDs)19, thereby reducing the side effects of antibody-based therapeutics.

    New tumor-selective light treatment could kill breast cancer cells with greater accuracy and improve tumor control

    This is a nontoxic version of cancer treatment that works on any type of cancer.


    Breast cancer is the most common cancer affecting women in Singapore. Treatment is multimodal and often involves surgery to remove the cancer and lymph nodes involved.

    Adjuvant therapy, given after the , is used to irradiate and destroy micrometastases, which are in the blood stream or lymphatics, to decrease recurrence. This form of therapy is subdivided into local (radiotherapy) and systemic therapy (endocrine therapy, chemotherapy and targeted therapy).

    Studies have shown that has increased with breast conserving therapy (BCT) where only the tumor and a margin is removed from the body post mastectomy, compared to full mastectomy alone, which removes all parts of the breast. For BCT, radiotherapy has to be administered after lumpectomy, which removes other from the breast and some normal tissue around it.

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    Proteins Predict Signs of Alzheimer’s Disease

    Protein indicators of subclinical peripheral heath in plasma were linked with markers of Alzheimer’s disease and neurodegeneration, cross-sectional proteomic analyses showed.

    Greater protein-based risk for cardiovascular disease, heart failure mortality, and kidney disease was associated with plasma biomarkers of amyloid-beta, phosphorylated tau181 (p-tau181), neurofilament light (NfL, a measure of neuronal injury), and glial fibrillary acidic protein (GFAP, a measure of astrogliosis), even in people without cardiovascular or kidney disease, reported Keenan Walker, PhD, of the National Institute on Aging in Baltimore, and co-authors.

    Proteomic indicators of body fat percentage, lean body mass, and visceral fat also were tied to p-tau181, NfL, and GFAP, Walker and colleagues wrote in the Annals of Neurology.

    You Are When You Eat

    The sleep-wake cycle is among the most well-known circadian rhythms in the body and is severely affected in Alzheimer’s disease (AD). “Eighty percent of patients with AD suffer dysregulation or disruption of circadian rhythms, and the obvious clinical manifestations are the sleep-wake reversals,” Desplats said. “These patients are very sleepy during the day, agitated during the night, more confused, and sometimes aggressive.”

    The feeding-fasting cycle is one of the strongest signals you can send the body to entrain the circadian clock.-Paula Desplats, University of California, San Diego

    In a recent study published in Cell Metabolism, Desplats’s team used mice that are genetically engineered to develop AD to test whether intermittent fasting improves circadian rhythm abnormalities.3 Rather than restricting calories or making dietary changes, they simply limited food access to a defined six-hour daily window. They found that time-restricted eating improved sleep, metabolism, memory, and cognition, and reduced brain amyloid deposits and neuroinflammatory gene expression. “Many of the genes that are affected in AD are rhythmically expressed in the brain, meaning that they are in direct relation with the circadian clock and are involved in functions that are fundamental to AD pathology,” Desplats said. Intermittent fasting restored the rhythmic activity of these genes, but the real surprise was the extent to which it mitigated brain amyloid deposits and improved cognition and sleep-wake behaviors. “I didn’t expect that it will have such a dramatic impact on pathology,” Desplats said.

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