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Men carrying two copies of a common genetic variant face double the risk of dementia, according to new findings from the ASPREE trial. New research has uncovered that men who carry a common genetic variant are twice as likely to develop dementia in their lifetime compared to women. The study.

The researchers are especially interested in how our bodies maintain balance. Metabolic homeostasis, the fancy term for it, may have shaped more traits than we realize.

And as diets continue to change today, our ancient genetic choices could still be nudging us in new directions.

The study is published in the journal Cell Genomics.

We are currently facing the possibility of achieving immortality for humans by 2030. This prediction comes from renowned futurist Ray Kurzweil, who has a history of making accurate predictions. He anticipates that with the ongoing progress in genetics, robotics, and nanotechnology, we will soon have nanobots coursing through our bloodstream, which could enable us to live forever. It’s truly remarkable to consider that this could be a reality within just seven years.

Nanobots, which are small robots sized between 50–100 nm in width, are currently being used in various clinical medical applications. They are used in research as DNA probes, imaging materials for cells, and targeted delivery vehicles for cells. According to Kurzweil, nanobots represent the future of medicine.

They will be capable of repairing our bodies at a cellular level, making us resistant to diseases, aging, and, ultimately death. Additionally, he theorizes that humans may be able to transfer their consciousness into digital form, leading to immortality.

Ischaemic heart disease remains the main cause of death worldwide. 1 Within its multifactorial aetiology low-density lipoprotein (LDL) and other apolipoprotein (apo) B-containing lipoproteins play a central, causal role, promoting the development of the underlying process of atherosclerosis. The use of statins and other drugs—ezetimibe, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors, bempedoic acid—to lower LDL is a central strategy in the prevention of atherosclerotic cardiovascular disease (ASCVD) in both primary and secondary settings. 2 However, in many individuals, a substantial ASCVD risk remains after LDL-cholesterol (LDL-C) goal achievement, and elevated plasma triglyceride (TG) is recognised as an important component of this residual risk. 3 Plasma TG, or more specifically TG-rich lipoproteins (TRL), is therefore an additional target for lipid-lowering therapy. Outcome studies of TG lowering using classical drugs such as fibrates and high-dose niacin when added to statins failed to demonstrate further ASCVD risk reduction, although retrospective analyses suggest that subgroups characterised by high TG and low high-density lipoprotein (HDL) may have positive results. 4–7 An alternative approach, treatment with high-dose eicosapentaenoic acid (EPA), has been shown to reduce cardiovascular risk in patients with (and without) hypertriglyceridaemia who are on statins. 8–10

This review explores the concepts behind, and practical implementation of, an evidence-based therapeutic strategy that tailors further intervention according to the plasma lipid profile in patients on standard statin therapy who are often undertreated. 11

Genetic analyses provide robust evidence that elevated TG is a causal risk factor for ASCVD 12 13 and underpin the finding from epidemiological studies that raised TG levels are positively and linearly related to cardiovascular risk (figure 1A). 14 15 The importance of these observations is that they reveal an often unaddressed major risk factor that is of particular relevance in people with obesity or type 2 diabetes in whom TG levels are frequently elevated. 16 Further, outcome trials have shown that elevated TG levels (again especially in type 2 diabetics) are associated with high residual cardiovascular risk in statin-treated patients with established cardiovascular disease, even if they have well-controlled LDL-C. 17–19.

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(Philadelphia, PA) – A single injection of a novel CRISPR gene-editing treatment safely and efficiently removes SIV – a virus related to the AIDS-causing agent HIV – from the genomes of non-human primates, scientists at the Lewis Katz School of Medicine at Temple University now report. The groundbreaking work complements previous experiments as the basis for the first-ever clinical trial of an HIV gene-editing technology in human patients, which was authorized by the Food and Drug Administration (FDA) in 2022.

The preclinical study, published online in the journal Gene Therapy, tested EBT-001, an SIV-specific CRISPR-Cas9 gene-editing therapy, in rhesus macaques. The study shows that EBT-001 effectively excises SIV from reservoirs – cells and tissues where viruses like SIV and HIV integrate into host DNA and hide for years – without any detectable off-target effects in animals. The work is a significant advance in the generation of a cure for HIV/AIDS in humans.

“Our study supports safety and demonstrates evidence of in vivo SIV editing of a CRISPR gene-editing technology aimed at the permanent inactivation of virus in a broad range of tissues in a large, preclinical animal model, using a one-time injection of the treatment,” said Kamel Khalili, PhD, Laura H. Carnell Professor and Chair of the Department of Microbiology, Immunology, and Inflammation, Director of the Center for Neurovirology and Gene Editing, Director of the Comprehensive NeuroAIDS Center at the Lewis Katz School of Medicine, and senior investigator on the new study.

Whether you are lucky enough to have a cat companion or must merely live this experience vicariously through cat videos, Felis catus is a familiar and comforting presence in our daily lives. Unlike most other feline species, cats exhibit sociality, can live in groups, and communicate both with other cats and humans, which is why they have been humans’ trusted accomplices for millennia.

Despite this intimacy, there is still much that we don’t know about our feline friends. Numerous behavioral studies have been conducted on other mammal species, but relatively few on cats.

In part to fill this gap, a team of researchers at the Wildlife Research Center of Kyoto University are investigating the genetic background of cats’ behavioral traits. Specifically, they aim to understand the association between traits like purring and variation in the androgen receptor gene. Though the exact function of purring remains unclear, previous studies have indicated that it is beneficial for feline communication and survival.

Chinese researchers have developed a technology that sheds light on how the three-dimensional (3D) organization of plant genomes influences gene expression—especially in photosynthesis.

The research, which was led by Prof. Xiao Jun at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences, in collaboration with BGI Research, is published in Science Advances.

The innovative method not only provides a more precise tool for understanding the intricate 3D interactions between genes, but also highlights the critical role of long-range chromatin interactions in gene regulation.

In a diseased condition, most of the time, target proteins attain toxicity following their transition from a α-helix to a β-sheet form [18]. Although numerous functional native proteins possess β-sheet conformations within them, the transition from an α-helix to a β-sheet is characteristic of amyloid deposits [19], and often associated with the change of a physiological function to a pathological one. Such abnormal conformational transition exposes hydrophobic amino acid residues and promotes protein aggregation [18, 20]. The toxic proteins often interact with other native proteins and may catalyze their transition into a toxic sate, and hence they are called infective conformations [18]. The newly formed toxic proteins can repeat this cycle to intiate a self-sustaining loop; thereby amplifying the toxicity to generate a catastrophic effect, beyond homeostatic reparative mechanisms, to eventually impair cellular function or induce cellular demise [21].

Proteins function properly when their constituent amino acids fold correctly [22]. On the other hand, misfolded proteins assemble into insoluble aggregates with other proteins and can be toxic for the cells [18, 20]. Ataxin-1 is highly prone to misfolding due to inherited gene defects that cause neurodegenerative diseases (NDDs), which is mainly due the repetition of glutamine within its amino acid chain; the toxicity of this protein being directly proportional to the number of glutamines [23]. There are 21 proteins that mainly interact with ataxin-1 and influence its folding or misfolding, 12 of which increase the toxicity of ataxin-1 for nerve cells, while 9 of the identified proteins reduce its toxicity [23]. Ataxin-1 resembles a double twisted spiral or helix and has a special structure, termed a “coiled coil domain”, that promotes aggregation. Proteins which possess “coiled coil domain” and interact with ataxin-1 have been reported to enhance promotion of ataxin-1 aggregation and toxic effects [24].

The gradual accumulation of misfolded proteins in the absence of their appropriate clearance can cause amyloid disease, the most prevalent one being AD. Parkinson’s disease and Huntington’s disease have similar amyloid origins [25]. These diseases can be sporadic or familial and their incidence increases dramatically with age. The mechanistic explanation for this correlation is that as we age (and are subjected to increasing numbers of mutations and/or oxidative stress causing changes to protein structure, etc.), the delicate balance of the synthesis, folding, and degradation of proteins is disturbed, ensuing in the production, accumulation and aggregation of misfolded proteins [26].