Lifeboat Foundation

Summary: Research reveals that people with high blood pressure who also sleep less than six hours per night face increased risks of brain injury, accelerated brain aging, and impaired executive function. The study assessed 682 participants from the Framingham Heart Study, analyzing sleep patterns, blood pressure, cognitive performance, and brain MRIs.

These risks were not present in individuals with normal blood pressure, highlighting a concerning interaction between sleep deprivation and hypertension. Researchers suggest treating sleep problems and hypertension as potential interventions to protect brain health and delay cognitive decline.

Researchers at The Hospital for Sick Children (SickKids) have uncovered that stress changes how our brain encodes and retrieves aversive memories, and discovered a promising new way to restore appropriate memory specificity in people with post-traumatic stress disorder (PTSD).

If you stumble during a presentation, you might feel stressed the next time you have to present because your brain associates your next presentation with that one poor and aversive experience. This type of stress is tied to one memory.

But stress from traumatic events like violence or generalized anxiety disorder can spread far beyond the original event, known as stress-induced aversive memory generalization, where fireworks or car backfires can trigger seemingly unrelated fearful memories and derail your entire day. In the case of PTSD, it can cause much greater negative consequences.

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🧑🏻‍🔬 By Ms. Cloe García Porta, Dr. Kashif Mahfooz, Mr. Joanna Komorowska, Dr. Sara Garcia-Rates and Dr. Susan Greenfield.

Continue reading “A Novel 14mer Peptide Inhibits Autophagic Flux via Selective Activation of the mTORC1 Signalling Pathway: Implications for Alzheimer’s Disease” »

A groundbreaking study has used patient-derived stem cells to recreate a rare genetic form of autism in the lab.

A new way of mapping activity and connections between different regions of the brain has revealed fresh insights into how higher order functions like language, thought and attention, are organized.

Traditional models of human brain activity represent interactions in pairs between two different brain regions. This is because modeling methods have not developed sufficiently to describe more complex interactions between multiple regions.

A new approach, developed by researchers at the University of Birmingham is capable of taking signals measured through neuroimaging, and creating accurate models from these to show how different brain regions are contributing to specific functions and behaviors. The results are published in Nature Communications.

Cleveland Clinic Genome Center researchers have unraveled how immune cells called microglia can transform and drive harmful processes like neuroinflammation in Alzheimer’s disease. The study, published in the journal Alzheimer’s & Dementia, also integrates drug databases with real-world patient data to identify FDA-approved drugs that may be repurposed to target disease-associated microglia in Alzheimer’s disease without affecting the healthy type.

The researchers, led by study corresponding author Feixiong Cheng, Ph.D., hope their unique approach of integrating genetic, chemical and human health data to identify drug targets and corresponding drugs will inspire other scientists to take similar approaches in their own research.

Microglia are specialized immune cells that patrol our brains, seeking and responding to tissue damage and external threats like bacteria and viruses. Different types of microglial cells use different methods to keep the brain safe. Some may cause neuroinflammation—inflammation in the brain—to fight invaders or kickstart the repair process in damaged cells. Others may work to “eat” dangerous substances in the brain, and clean up damage and debris. However, during Alzheimer’s disease, new types of microglia can form that promote disease progression.

Chaperone-mediated autophagy (CMA) is the lysosomal degradation of individually selected proteins, independent of vesicle fusion. CMA is a central part of the proteostasis network in vertebrate cells. However, CMA is also a negative regulator of anabolism, and it degrades enzymes required for glycolysis, de novo lipogenesis, and translation at the cytoplasmic ribosome. Recently, CMA has gained attention as a possible modulator of rodent aging. Two mechanistic models have been proposed to explain the relationship between CMA and aging in mice. Both of these models are backed by experimental data, and they are not mutually exclusionary. Model 1, the “Longevity Model,” states that lifespan-extending interventions that decrease signaling through the INS/IGF1 signaling axis also increase CMA, which degrades (and thereby reduces the abundance of) several proteins that negatively regulate vertebrate lifespan, such as MYC, NLRP3, ACLY, and ACSS2. Therefore, enhanced CMA, in early and midlife, is hypothesized to slow the aging process. Model 2, the “Aging Model,” states that changes in lysosomal membrane dynamics with age lead to age-related losses in the essential CMA component LAMP2A, which in turn reduces CMA, contributes to age-related proteostasis collapse, and leads to overaccumulation of proteins that contribute to age-related diseases, such as Alzheimer’s disease, Parkinson’s disease, cancer, atherosclerosis, and sterile inflammation. The objective of this review paper is to comprehensively describe the data in support of both of these explanatory models, and to discuss the strengths and limitations of each.

Chaperone-mediated autophagy (CMA) is a highly selective form of lysosomal proteolysis, where proteins bearing consensus motifs are individually selected for lysosomal degradation (Dice, 1990; Cuervo and Dice, 1996; Cuervo et al., 1997). CMA is mechanistically distinct from macroautophagy and microautophagy, which, along with CMA, are present in most mammalian cells types.

Macroautophagy (Figure 1 A) begins when inclusion membranes (phagophores) engulf large swaths of cytoplasm or organelles, and then seal to form double-membrane autophagosomes. Autophagosomes then fuse with lysosomes, delivering their contents for degradation by lysosomal hydrolases (Galluzzi et al., 2017). Macroautophagy was the first branch of autophagy to be discovered, and it is easily recognized in electron micrograms, based on the morphology of phagophores, autophagosomes, and lysosomes (Galluzzi et al., 2017).

Understanding neonatal brain injury — can it teach us about adult-onset neurodegenerative disease?

A new laboratory study in mice suggests that primates like humans evolved large brains with a helping hand from microbes that live in the gut.