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Results of DNA studies also seem to confirm the idea that optimism is an effective tool for slowing down cellular aging, of which telomere shortening is a biomarker. (Telomeres are the protective caps at the end of our chromosomes.) This research is still in progress, but the early results are informative. In 2012, Elizabeth Blackburn, who three years earlier shared a Nobel Prize for her work in discovering the enzyme that replenishes the telomere, and Elissa Epel at the University of California at San Francisco, in collaboration with other institutions, identified a correlation between pessimism and accelerated telomere shortening in a group of postmenopausal women. A pessimistic attitude, they found, may indeed be associated with shorter telomeres. Studies are moving toward larger sample sizes, but it already seems apparent that optimism and pessimism play a significant role in our health as well as in the rate of cellular senescence. More recently, in 2021, Harvard University scientists, in collaboration with Boston University and the Ospedale Maggiore in Milan, Italy, observed the telomeres of 490 elderly men in the Normative Health Study on U.S. veterans. Subjects with strongly pessimistic attitudes were associated with shorter telomeres — a further encouraging finding in the study of those mechanisms that make optimism and pessimism biologically relevant.

Optimism is thought to be genetically determined for only 25 percent of the population. For the rest, it’s the result of our social relationships or deliberate efforts to learn more positive thinking. In an interview with Jane Brody for the New York Times, Rozanski explained that “our way of thinking is habitual, unaware, so the first step is to learn to control ourselves when negative thoughts assail us and commit ourselves to change the way we look at things. We must recognize that our way of thinking is not necessarily the only way of looking at a situation. This thought alone can lower the toxic effect of negativity.” For Rozanski, optimism, like a muscle, can be trained to become stronger through positivity and gratitude, in order to replace an irrational negative thought with a positive and more reasonable one.

While the exact mechanisms remain under investigation, a growing body of research suggests that optimism plays a significant role in promoting both physical and mental well-being. Cultivating a positive outlook, then, can be a powerful tool for fostering resilience, managing stress, and potentially even enhancing longevity. By adopting practices that nurture optimism, we can empower ourselves to navigate life’s challenges with greater strength and live healthier, happier lives.

A novel approach in the field of Alzheimer’s research is emerging that could potentially transform how we tackle this debilitating disease. Recent studies have revealed a paradigm shift in understanding Alzheimer’s pathology, emphasizing the importance of targeting the early-stage aggregation of the pathogenic amyloid beta (A-beta) protein, specifically focusing on its soluble oligomeric form.

Over the past three decades, conventional treatments for Alzheimer’s have largely been ineffective, primarily due to their focus on combating the fibrillar form of A-beta. However, emerging research suggests that it is the soluble oligomeric form of A-beta that poses the greatest threat to neuronal health, leading to cognitive decline and neurotoxicity.

A recent breakthrough in Alzheimer’s treatment has come from the development of an antibody capable of recognizing both oligomeric and fibrillar forms of A-beta, offering newfound hope to the field. This innovative therapy has demonstrated promising results in delaying disease progression by up to 36% in individuals with early-to-mild cognitive impairment.

Researchers report that lipid droplets in brain cells may be a more significant factor in the development of Alzheimer’s disease than previously thought.

Human brains preserve in diverse environments for at least 12 000 years—new research in Proceedings B this week: https://royalsocietypublishing.org/doi/10.1098/rspb.2023.

Soft tissue preservation in the geological record is relatively rare, and when an archaeologist digs a human skull out of the…

The brain is thought to be among the first human organs to decompose after death. The discovery of brains preserved in the archaeological record is therefore regarded as unusual. Although mechanisms such as dehydration, freezing, saponification, and tanning are known to allow for the preservation of the brain on short time scales in association with other soft tissues (≲4000 years), discoveries of older brains, especially in the absence of other soft tissues, are rare. Here, we collated an archive of more than 4,400 human brains preserved in the archaeological record across approximately 12 000 years, more than 1,300 of which constitute the only soft tissue preserved amongst otherwise skeletonized remains. We found that brains of this type persist on time scales exceeding those preserved by other means, which suggests an unknown mechanism may be responsible for preservation particular to the central nervous system. The untapped archive of preserved ancient brains represents an opportunity for bioarchaeological studies of human evolution, health and disease.

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How do multiple synapses interact to modulate learning? Agnes and Vogels postulate models of ‘co-dependent’ synaptic plasticity that promote rapid, multi-synaptic attainment of stable receptive fields, dendritic patterns and plausible neural dynamics.

Studies of brain network connectivity improved understanding on brain changes and adaptation in response to different pathologies. Synaptic plasticity, the ability of neurons to modify their connections, is involved in brain network remodeling following different types of brain damage (e.g., vascular, neurodegenerative, inflammatory). Although synaptic plasticity mechanisms have been extensively elucidated, how neural plasticity can shape network organization is far from being completely understood. Similarities existing between synaptic plasticity and principles governing brain network organization could be helpful to define brain network properties and reorganization profiles after damage. In this review, we discuss how different forms of synaptic plasticity, including homeostatic and anti-homeostatic mechanisms, could be directly involved in generating specific brain network characteristics. We propose that long-term potentiation could represent the neurophysiological basis for the formation of highly connected nodes (hubs). Conversely, homeostatic plasticity may contribute to stabilize network activity preventing poor and excessive connectivity in the peripheral nodes. In addition, synaptic plasticity dysfunction may drive brain network disruption in neuropsychiatric conditions such as Alzheimer’s disease and schizophrenia. Optimal network architecture, characterized by efficient information processing and resilience, and reorganization after damage strictly depend on the balance between these forms of plasticity.

Keywords: brain networks, connectivity, synaptic plasticity, Alzheimer’s disease (AD), schizophrenia, long-term potentiation (LTP), synaptic scaling, resting state functional MRI (rs-fMRI)

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Our H+ friend Rob Wilkes alerted me to this today!

March 20 (Reuters) — Elon Musk’s brain-chip startup Neuralink livestreamed on Wednesday its first patient implanted with a chip using his mind to play online chess.

Noland Arbaugh, the 29-year-old patient who was paralyzed below the shoulder after a diving accident, played chess on his laptop and moved the cursor using the Neuralink device. The implant seeks to enable people to control a computer cursor or keyboard using only their thoughts.

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Neuralink, Elon Musk ’s brain chip startup, released a video on Wednesday showing the company’s first patient using a laptop with just his mind.

The video, which was livestreamed on Neuralink’s account on X, showed 29-year-old Noland Arbaugh playing a game of chess on his laptop using Neuralink’s brain computer interface (BCI) technology. Arbaugh is paralyzed from the shoulders down due to what he describes as a “freak diving accident.”

“It’s all brain power there,” Arbaugh said, referring to his ability to use a mouse and keyboard unassisted. He later added, “Basically, it was like using the Force on the cursor and I could get it to move wherever I wanted.”

The immune system is comprised of two separate responses referred to as either innate or adaptive immunity. Both work in collaboration to elicit protection against anything the body encounters as ‘foreign’. In many cases foreign pathogens that enter the body are recognized by the innate immune system first which then activate adaptive immunity. The innate immune system uses many broad, non-specific cells to detect anything that might cause harm to the body. These cells initiate inflammation and the overall immune response. The adaptive immune system comes second and is more specific to the invading pathogen. Adaptive immune cells can not only help lyse or kill the invaders, but also generate cells to ‘remember’ that pathogen in the future. This is a common phenomenon that occurs when we overcome an illness and is known as immunological memory. Vaccine biology is based on this concept that we will generate ‘memory cells’ in response to attenuated viruses.

The study of immunity and how our body fights off disease is a progressively growing field. Currently, scientists know many of the key players that drive this immunological memory. However, researchers and physicians are working together to better understand this process and how to generate more effective treatments for various diseases. An exciting article in Nature, published by Dr. Francisco J. Quintana and others, demonstrate that a glial cell can generate immunological memory. Quintana, an investigator at Brigham and Women’s Hospital, and his team study different signaling pathways associated with immune activity to identify novel therapeutic treatments and biomarkers to measure treatment efficacy. The glial cell Quintana and his team found to aid in immunity is known as an astrocyte, which is a key cell within the central nervous system (CNS). Astrocytes help promote synapse formation, clear excess neurotransmitters, and maintain the blood-brain barrier.

For the first time astrocytes have been connected to obtain memory-like properties and aid in immunity. The team used multiple models to demonstrate that astrocytes can remember previous interactions with immune cells. Not only did this function improve response time to infection but induced a stronger immune response when re-exposed to the same disease. Due to similarities in memory formation, Quintana and others refer to this process as ‘astrocyte immune memory’. Interestingly, due to astrocytes long lifespan, these cells could provide insight into chronic neurologic disorders.