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Summary: Study uncovers new genetic risk factors for age-related macular degeneration, a leading cause of vision loss in adults.

Source: PLOS

Combining a map of gene regulatory sites with disease-associated loci has uncovered a new genetic risk factor of adult-onset macular degeneration (AMD), according to a new study publishing January 17 in the open-access journal PLOS Biology by Ran Elkon and Ruth Ashery-Padan of Tel Aviv University, Israel, and colleagues.

Researchers at Chalmers University of Technology have made a ground-breaking discovery in the field of synthetic DNA, using AI to control the cells’ protein production.

This new technology could revolutionize the way we produce vaccines, drugs for severe diseases, and alternative food proteins by making the process faster and significantly cheaper than current methods.

The process of gene expression is fundamental to the function of cells in all living organisms. In simple terms, the genetic code in DNA is transcribed into the molecule messenger RNA (mRNA), which tells the cell’s factory which protein to produce and in what quantities.

A study by the HSE Centre for Language and Brain has confirmed the role of the corpus callosum in language lateralization, the distribution of language processing functions between the brain’s hemispheres. The authors came up with an innovative language task for their study subjects and applied advanced neuroimaging methods to the data collected. A paper on their findings has been published in PLoS ONE.

Functional asymmetry between the two cerebral hemispheres in performing higher-level cognitive functions is a major characteristic of the human brain. For example, the left hemisphere plays a leading role in language processing in most people. However, between 10% and 15% of the human population also use the right hemisphere to varying degrees for the same task.

Traditionally, language lateralization to the right hemisphere was explained by handedness, as it is mainly found in left-handed and ambidextrous (using both hands equally well) individuals. But recent research has demonstrated a genetic difference in the way language is processed by left-handed and ambidextrous people. In addition to this, some right-handed people also involve their right hemisphere in language functions.

Scientists at Harvard Medical School have investigated why we age, and identified a possible way to reverse it. In tests in mice, the team showed that epigenetic “software glitches” drive the symptoms of aging – and a system reboot can reverse them, potentially extending lifespan.

Our genome contains our complete DNA blueprint, which is found in every single cell of our bodies. But it’s not the whole picture – an extra layer of information, known as the epigenome, sits above that and controls which genes are switched on and off in different types of cells. It’s as though every cell in our body is working from the same operating manual (the genome), but the epigenome is like a table of contents that directs different cells to different chapters (genes). After all, lung cells need very different instructions to heart cells.

Environmental and lifestyle factors like diet, exercise and even childhood experiences could change epigenetic expression over our lifetimes. Epigenetic changes have been linked to the rate of biological aging, but whether they drove the symptoms of aging or were a symptom themselves remained unclear.

Chromatin structures and transcriptional networks are known to specify cell identity during development which directs cells into metaphorical valleys in the Waddington landscape. Cells must retain their identity through the preservation of epigenetic information and a state of low Shannon entropy for the maintenance of optimal function. Yeast studies in the 1990s have reported that a loss of epigenetic information compared to genetics can cause aging. Few other studies also confirmed that epigenetic changes are not just a biomarker but a cause of aging in yeasts.

Epigenetic changes associated with aging include changes in DNA methylation (DNAme) patterns, H3K27me3, H3K9me3, and H3K9me3. Many epigenetic changes have been observed to follow a specific pattern. However, the reason for changes in the mammalian epigenome is not yet known. A few clues can be obtained from yeast, where DSB is a significant factor whose repair requires epigenetic regulators Esa1, Gcn5, Rpd3, Hst1, and Sir2. As per the ‘‘RCM’’ hypothesis and ‘Information Theory of Aging’’, aging in eukaryotes occurs due to the loss of epigenetic information and transcriptional networks in response to cellular damage such as a crash injury or a DSB.

A new study in the journal Cell aimed to determine whether epigenetic changes are a cause of mammalian aging.

A new study led by scientists at Rutgers University has uncovered new insights into the underlying brain mechanisms of autism spectrum disorder.

Autism Spectrum Disorder (ASD) is a complex developmental disorder that affects how a person communicates and interacts with others. It is characterized by difficulty with social communication and interaction, as well as repetitive behaviors and interests. ASD can range from mild to severe, and individuals with ASD may have a wide range of abilities and challenges. It is a spectrum disorder because the symptoms and characteristics of ASD can vary widely from person to person. Some people with ASD are highly skilled in certain areas, such as music or math, while others may have significant learning disabilities.

Bats (Mammalia: Chiroptera) serve as natural reservoirs for many zoonotic pathogens worldwide, including vector-borne pathogens. However, bat-associated parasitic arthropods and their microbiota are thus far not thoroughly described in many regions across the globe, nor is their role in the spillover of pathogens to other vertebrate species well understood. Basic epidemiological research is needed to disentangle the complex ecological interactions among bats, their specific ectoparasites and microorganisms they harbor. Some countries, such as Ukraine, are particularly data-deficient in this respect as the ectoparasitic fauna is poorly documented there and has never been screened for the presence of medically important microorganisms. Therefore, the aims of this study were to provide first data on this topic.

A total of 239 arthropod specimens were collected from bats. They belonged to several major groups of external parasites, including soft ticks, fleas, and nycteribiid flies from six chiropteran species in Northeastern Ukraine. The ectoparasites were individually screened for the presence of DNA of Rickettsia spp., Anaplasma/Ehrlichia spp., Bartonella spp., Borrelia spp., and Babesia spp. with conventional PCRs. Positive samples were amplified at several loci, sequenced for species identification, and subjected to phylogenetic analysis.

Rickettsia DNA was detected exclusively in specimens of the soft tick, Carios vespertilionis (7 out of 43 or 16.3%). Sequencing and phylogenetic analysis revealed high similarity to sequences from Rickettsia parkeri and several other Rickettsia species. Bacteria from the family Anaplasma taceae were detected in all groups of the ectoparasites (51%, 122/239 samples), belonging to the genera Anaplasma, Ehrlichia, and Wolbachia. The detection of Bartonella spp. was successful only in fleas (Nycteridopsylla eusarca) and bat flies (Nycteribia koleantii, N. pedicularia), representing 12.1% (29÷239) of the collected ectoparasites. No DNA of Babesia or Borrelia species was identified in the samples.

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Excessive fear is a hallmark of anxiety disorders, a major cause of disease burden worldwide. Substantial evidence supports a role of prefrontal cortex-amygdala circuits in the regulation of fear and anxiety, but the molecular mechanisms that regulate their activity remain poorly understood. Here, we show that downregulation of the histone methyltransferase PRDM2 in the dorsomedial prefrontal cortex enhances fear expression by modulating fear memory consolidation. We further show that Prdm2 knock-down (KD) in neurons that project from the dorsomedial prefrontal cortex to the basolateral amygdala (dmPFC-BLA) promotes increased fear expression. Prdm2 KD in the dmPFC-BLA circuit also resulted in increased expression of genes involved in synaptogenesis, suggesting that Prdm2 KD modulates consolidation of conditioned fear by modifying synaptic strength at dmPFC-BLA projection targets.