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Scientists discover a new pathway to long-term memory formation in the brain that can bypass the formation of short-term memory.

Scientists Reveal Direct Path to Long-Term Memory Formation, Bypassing Short-Term Memory

Brain music illustration

Brain’s Musical Rhythm and Language Skills Share Deep Genetic Roots

infographic

AI Outpaces Brain Experts at Predicting Study Results

MIT scientists find that motor neuron growth increased significantly over 5 days in response to biochemical (left) and mechanical (right) signals related to exercise. The green ball represents cluster of neurons that grow outward in long tails, or axons.

Neurons Grow Faster When Muscles Exercise, MIT Study Reveals

Suspicious protein molecules and fibrils aggregate on nerve cells in dementia. Illustration: Empa

Scientists Identify ‘Superspreader’ Proteins That May Drive Alzheimer’s Progression

visual clutter illustration (Illustration by Michael S. Helfenbein)

Visual Clutter Disrupts Brain’s Information Processing, Yale Study Reveals

Neha Sapkal does research to understand the neural code of stopping in the fly.

HALT! Scientists decode brain mechanisms of stopping

Drawing of a camera and photos

New Study Reveals How Emotion Can Boost Memory for Contextual Details, Challenging Long-Held Beliefs

myhero zero main character

How the brain processes the number zero

Researchers at WashU Medicine have developed a method in mice to reduce damage from spinal cord injuries by using engineered immune cells. Mice that received this treatment showed improved recovery from their injuries, indicating potential for developing this therapy for human use.

New Discovery Could Help Fine-Tune Scarring in Spinal Cord Injuries

Neurons. Alzheimer’s disease varies widely in its age of onset, presentation, and severity. Recently, the SORL1 gene has received increased attention since variations in this gene have been associated with both early- and late-onset Alzheimer’s. However, little is known about how damage to SORL1 leads to disease. Using stem cells from patients with Alzheimer’s, investigators from Harvard-affiliated Brigham and Women’s Hospital found that loss of normal SORL1 function leads to a reduction in two key proteins known to be involved in Alzheimer’s and which play an essential role in the neurons of healthy individuals. Their results, published in Cell Reports, suggest a potential strategy for Alzheimer’s disease treatment, especially for patients not responsive to existing therapies. In this new study, the researchers utilized a stem-cell based approach that examined natural genetic variability in Alzheimer’s patients to gain insight into an alternative pathway driving disease. The researchers used CRISPR technologies to remove the SORL1 gene from progenitor stem cells, derived from participants in two Alzheimer’s research cohorts, the Religious Order Studies and Rush Memory and Aging Project. They then programmed the stem cells to differentiate into four different kinds of brain cells to examine the impact of removing SORL1 on each cell type. The most dramatic impact was seen in neurons and a “support” cell in the brain (astrocytes). Neurons lacking SORL1 demonstrated especially prominent reduction in the levels of two key Alzheimer’s disease proteins: APOE and CLU. Without APOE and CLU, neurons cannot properly regulate lipids, which accumulate in droplets that may impair neurons’ abilities to communicate with each other. The researchers verified their lab-based results by examining natural genetic variation in SORL1 expression in the brain tissue of 50 members of the cohorts, finding again that lower SORL1 activity in neurons was correlated with reduced APOE and CLU in these people. Historically, researchers have studied three potent genetic drivers of Alzheimer’s disease (APP, PSEN1 and PSEN2), which are commonly mutated in hereditary, early-onset Alzheimer’s (AD diagnosis before age 65). Preclinical models and cell-based systems largely rely on mutations in these genes to model Alzheimer’s disease, even though in many people with late-onset (“sporadic”) Alzheimer’s, a more complex interaction between genes, lifestyle, and environment determines the presentation of the disease. Key neurological features of Alzheimer’s disease, including the abundance of amyloid-beta plaques in the brain, also vary across individuals. “Our study is one of the first with human cells from a large collection of individuals to try to understand the ‘molecular road’ that starts with SORL1, which we now see converges with APOE,” said corresponding author Tracy Young-Pearse of the Ann Romney Center for Neurological Diseases. “Our research points to the importance of developing interventions that target these and other molecular roads to Alzheimer’s disease. The more we can understand subtype-specific differences in AD, the better we will be able to design rational therapeutic interventions to try to fix the problem that is primarily driving disease in each patient.” The researchers are continuing to study other pathways that may lead to Alzheimer’s disease, such as those involving microglia (brain cells that perform immune functions). By using study models and techniques reflective of Alzheimer’s disease presentation in the general population, the researchers hope to identify additional biological pathways important in Alzheimer’s disease. In addition, Brigham researchers have played a leadership role in understanding the molecular and genetic basis for Alzheimer’s disease, including making key discoveries related to the amyloid protein. Two novel anti-amyloid therapies, aducanumab and lecanemab, have received U.S. Food and Drug Administration accelerated and traditional approval, respectively, but not all patients respond to these drugs, warranting other treatment options. This work was supported by the National Institutes of Health (F31AG063399, U01AG072572, U01AG061356, RF1NS117446 and R01AG055909).

Study Unveils Shared Cellular Mechanisms in Major Dementias

New research from the University of Washington’s Institute for Learning & Brain Sciences, or I-LABS, found the COVID-19 pandemic lockdowns resulted in unusually accelerated brain maturation in adolescents. This maturation was more pronounced in females, as seen on the left.

COVID-19 Lockdowns Sped Up Brain Aging in Teens, Especially Girls

The image displays four views of a person's brain, highlighting the boundaries between different functional brain networks, each represented by different colored lines, as mapped using functional MRI. This map is overlaid on a salience network connectivity heat map, where warmer colors indicate stronger connectivity within the salience network. Researchers discovered that a larger salience network may be associated with an increased risk of depression. Credit: Lynch/Liston Labs.

Brain Scans Reveal Neuronal ‘Wiring’ Linked to Depression Risk

An astrocyte cell grown in tissue culture stained with antibodies to GFAP and vimentin. © GerryShaw / Wikipedia

Astrocytes Reprogrammed into Brain Stem Cells: A New Hope for Regenerative Medicine

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