Cats with dementia have brain changes similar to those of people with Alzheimer’s disease, offering a valuable model for studying the condition in humans, a study says.
Category: neuroscience – Page 260
Targeting Cellular Senescence: Pathophysiology in Multisystem Age-Related Diseases
With the intensification of global aging, the incidence of age-related diseases (including cardiovascular, neurodegenerative, and musculoskeletal disorders) has been on the rise, and cellular senescence is identified as the core driving mechanism. Cellular senescence is characterized by irreversible cell cycle arrest, which is caused by telomere shortening, imbalance in DNA damage repair, and mitochondrial dysfunction, accompanied by the activation of the senescence-associated secretory phenotype (SASP). In this situation, proinflammatory factors and matrix-degrading enzymes can be released, thereby disrupting tissue homeostasis. This disruption of tissue homeostasis induced by cellular senescence manifests as characteristic pathogenic mechanisms in distinct disease contexts. In cardiovascular diseases, senescence of cardiomyocytes and endothelial cells can exacerbate cardiac remodeling.
Stem cell-derived dopamine neurons improve depression-like behaviors in mice
The Institute of Neuroscience, Chinese Academy of Sciences, reports that human stem cell-derived A10-like midbrain dopaminergic neurons integrate into mouse mesocorticolimbic circuits and suppress anxiety and depression behaviors upon activation.
Midbrain dopaminergic neurons regulate voluntary movement, reward, motivation, cognition, and emotions. A10 ventral tegmental area neurons connect with nucleus accumbens, amygdala, olfactory tubercle, and medial prefrontal cortex. Dysfunction of the A10 system is implicated in drug addiction, schizophrenia, and depression.
Human pluripotent stem cells enable fresh production of disorder-relevant neurons, with previous success in enriching A9 neurons for Parkinson’s disease therapy. Efficient differentiation of human A10 dopaminergic neurons remains elusive.
Brain Autopsies Revealed a Potential Culprit Behind Alzheimer’s
Scientists have revealed that immune cells in Alzheimer’s brains behave differently from those in brains of people without the disease – a discovery that could lead to new treatments.
Published in 2023, an analysis of human brain tissue discovered microglia in the brains of people with Alzheimer’s were more frequently in a pre-inflammatory state, making them less likely to be protective.
Microglia are immune cells that help keep our brains healthy by clearing waste and preserving normal brain function.
Scientists just found a protein that reverses brain aging
Scientists at UCSF have uncovered a surprising culprit behind brain aging: a protein called FTL1. In mice, too much FTL1 caused memory loss, weaker brain connections, and sluggish cells. But when researchers blocked it, the animals regained youthful brain function and sharp memory. The discovery suggests that one protein could be the master switch for aging in the brain — and targeting it may one day allow us to actually reverse cognitive decline, not just slow it down.
Blocking brain damage may slow glioblastoma growth
Blocking brain damage triggered by a glioblastoma, an aggressive brain cancer, may slow the growth of the cancer and allow the brain to keep working better for longer, according to a new study led by UCL (University College London) researchers.
The study, published in Nature, looked at glioblastomas in mice. It found that early-stage tumors damaged parts of nerve cells called axons, and that the brain’s natural response to this injury—breaking down and clearing away these damaged axons—accelerated the tumor’s growth.
Mice in whom this natural response was turned off developed less aggressive tumors, lived for longer and maintained normal brain function that persisted to nearly the end of their lives. In contrast, mice who responded to nerve damage as normal developed more aggressive tumors and progressive disability, the researchers found.
Changing how we understand, and potentially treat, misophonia
Throughout her career, Laurie Heller has listened closely—not just to words, but to sound itself. In the Auditory Lab at Carnegie Mellon University, the psychology professor explores how the brain interprets everything from environmental clatter to the subtle noises that can spark deep feelings of safety, connection, or in some cases, rage.
So when Yuqi “Monica” Qiu, then an undergraduate in computer science, emailed Heller after seeing a recruitment poster for a study, Heller was ready to listen.
“I have misophonia,” Qiu wrote. “And I want to help.”
Eye movement patterns reveal subtle signs of cognitive and memory decline
A multi-institution team across Canada and the West Indies reports that gaze patterns can serve as a sensitive marker of cognitive decline, with associated reductions in explorative, adaptive, and differentiated visual sampling of the environment.
Eye movements are closely linked to encoding and retrieval processes, with changes in viewing behavior often reflecting age and pathology-related memory declines. Previous work has noted that groups differing in memory status diverge across multiple gaze features, suggesting that univariate gaze metrics may not fully capture the complexity of memory-related viewing behaviors.
In the study, “Decoding memory function through naturalistic gaze patterns,” published in PNAS, researchers investigated changes in naturalistic viewing behavior across five participant groups to explore possible gaze-based indicators of memory function.