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Category: neuroscience – Page 14

Why some memories last a lifetime while others fade fast

Correlation alone could not answer the key questions, so co-lead Celine Chen created a CRISPR-based screening platform to alter gene activity in the thalamus and cortex. This approach showed that removing certain molecules changed how long memories lasted, and each molecule operated on its own timescale.

Timed Programs Guide Memory Stability

The results indicate that long-term memory relies not on a single on/off switch, but on a sequence of gene-regulating programs that unfold like molecular timers across the brain.

Speaking Multiple Languages May Slow Brain Aging, Study Suggests

People are living longer than ever around the world. Longer lives bring new opportunities, but they also introduce challenges, especially the risk of age-related decline.

Alongside physical changes such as reduced strength or slower movement, many older adults struggle with memory, attention and everyday tasks.

Researchers have spent years trying to understand why some people stay mentally sharp while others deteriorate more quickly. One idea attracting growing interest is multilingualism, the ability to speak more than one language.

Astrocytic Sox9 overexpression in Alzheimer’s disease mouse models promotes Aβ plaque phagocytosis and preserves cognitive function

Researchers at Baylor College of Medicine have discovered a natural mechanism that clears existing amyloid plaques in the brains of mouse models of Alzheimer’s disease and preserves cognitive function. The mechanism involves recruiting brain cells known as astrocytes, star shaped cells in the brain, to remove the toxic amyloid plaques that build up in many Alzheimer’s disease brains. Increasing the production of Sox9, a key protein that regulates astrocyte functions during aging, triggered the astrocytes’ ability to remove amyloid plaques. The study, published in Nature Neuroscience, suggests a potential astrocyte-based therapeutic approach to ameliorate cognitive decline in neurodegenerative disease.

“Astrocytes perform diverse tasks that are essential for normal brain function, including facilitating brain communications and memory storage. As the brain ages, astrocytes show profound functional alterations; however, the role these alterations play in aging and neurodegeneration is not yet understood,” said first author Dr. Dong-Joo Choi, who was at the Center for Cell and Gene Therapy and the Department of Neurosurgery at Baylor while he was working on this project. Choi currently is an assistant professor at the Center for Neuroimmunology and Glial Biology, Institute of Molecular Medicine at the University of Texas Health Science Center at Houston.

Astrocytes are associated with Alzheimer’s disease pathogenesis. We found that the transcription factor Sox9 functions to enhance astrocytic phagocytosis of Aβ plaques via MEGF10, and this clearance of plaques is associated with the preservation of cognitive function in mouse models.

Brain “stars” hold the power to preserve cognitive function in model of Alzheimer’s disease

Researchers at Baylor College of Medicine have discovered a natural mechanism that clears existing amyloid plaques in the brains of mouse models of Alzheimer’s disease and preserves cognitive function. The mechanism involves recruiting brain cells known as astrocytes, star shaped cells in the brain, to remove the toxic amyloid plaques that build up in many Alzheimer’s disease brains. Increasing the production of Sox9, a key protein that regulates astrocyte functions during aging, triggered the astrocytes’ ability to remove amyloid plaques. The study, published in Nature Neuroscience, suggests a potential astrocyte-based therapeutic approach to ameliorate cognitive decline in neurodegenerative disease.

“Astrocytes perform diverse tasks that are essential for normal brain function, including facilitating brain communications and memory storage. As the brain ages, astrocytes show profound functional alterations; however, the role these alterations play in aging and neurodegeneration is not yet understood,” said first author Dr. Dong-Joo Choi, who was at the Center for Cell and Gene Therapy and the Department of Neurosurgery at Baylor while he was working on this project. Choi currently is an assistant professor at the Center for Neuroimmunology and Glial Biology, Institute of Molecular Medicine at the University of Texas Health Science Center at Houston.

Astrocytic Sox9 overexpression in Alzheimer’s disease mouse models promotes Aβ plaque phagocytosis and preserves cognitive function.

Specialized neuron populations in the mouse cortex coordinate to guide correct decisions, study suggests

For decades, neuroscientists have been trying to pinpoint the neural underpinnings of behavior and decision-making. Past studies suggest that specialized groups of neurons in the mammalian brain, particularly in the cortex, work together to support decision-making and behavioral choices.

Some cortical neurons project to specific regions in the brain. This essentially means that they send axons, projections that transmit electrical impulses from one cell to another, to other areas.

Some neuroscientists have hypothesized that neurons projecting to the same area form specialized “population codes,” coordinated activity patterns that collectively represent specific information.

Humans may be born with preconfigured brains that help us understand the world

In a fascinating new study, scientists used pieces of human brain tissue to demonstrate that neural circuits produce electrical patterns very early in the development process, even before senses are active.

These experiments at the University of California, Santa Cruz (UCSC) and other labs suggest that the brain comes with built-in timing rules for thoughts.

Mitochondrial Dysfunction and Oxidative Stress in Alzheimer’s Disease

Mitochondrial ATP production by oxidative phosphorylation (OXPHOS) is essential for cellular functions, such that mitochondria are known as the powerhouses of the cell (Verschueren et al., 2019). The mitochondrial ETC consists of five enzyme complexes in the inner membrane of the mitochondria. ETC generates a charge across the inner mitochondrial membrane, which drives ATP synthase (complex V) to synthesize ATP from ADP and inorganic phosphate.

Several studies have shown impairments of all five complexes in multiple areas of the AD brain (Kim et al., 2000, 2001; Liang et al., 2008). Mitochondrial dysfunction in AD is apparent from a decrease in neuronal ATP levels, which is associated with the overproduction of ROS, and indicates that mitochondria may fail to maintain cellular energy. A substantial amount of ATP is consumed in the brain due to the high energy requirements of neurons and glia. Since an energy reserve (such as fat or glucose) is not available in the central nervous system (CNS), brain cells must continuously generate ATP to sustain neuronal function (Khatri and Man, 2013). Mitochondria are the primary source of cellular energy production, but aged or damaged mitochondria produce excess free radicals, which can reduce the supply of ATP and contribute to energy loss and mitochondrial dysfunction in AD. Importantly, oxidative damage of the promoter of the gene encoding subunit of the mitochondrial ATP synthase results in reduced levels of the corresponding protein, leading to decreased ATP production, nuclear DNA damage to susceptible genes, and loss of function (Lu et al., 2004; Reed et al., 2008).

In advanced stages of AD, substantial nitration of ATP synthase subunits can take place, leading to the irregular function of the respiratory chain (Castegna et al., 2003; Sultana et al., 2006; Reed et al., 2009). Likewise, ATP-synthase lipoxidation occurs in the hippocampus and parietal cortex of patients with mild cognitive impairment (Reed et al., 2008). Compromised OXPHOS contributes to a characteristic mitochondrial dysfunction in AD brains, leading to decreased ATP production, elevated oxidative stress, and ultimately cell death (Reddy, 2006; Reddy and Beal, 2008; Du et al., 2012). The specific mechanisms of OXPHOS deficiency in AD remain a long-standing scientific question, but the role of mitochondrial F1Fo ATP synthase dysfunction in AD-related mitochondrial OXPHOS failure is emphasized by emerging evidence (Beck et al., 2016; Gauba et al., 2019).

How the brain develops and resolves inflammation

Brain development is a complex process involving, for example, the precise diversification and distribution of cells into distinct areas. The researchers behind the present study have developed a new method called spatial tri-omics, that enables them to simultaneously measure in a specific area of the brain: 1) the activity of genes, 2) how this activity is regulated by epigenetic changes, and 3) if this activity ultimately leads to the production of proteins.

The study is based on analyses of mouse and human brains at different stages of development. The authors generated a spatiotemporal tri-omic atlas of the mouse brain from postnatal day 0 (P0) to P21 and compared corresponding regions with the human developing brain.

“We’ve been able to use this multidimensional method to track brain development over time and map changes from birth to a young age in different parts of the brain, as well as study how the brain reacts to inflammation,” explains the senior author.

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