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Category: neuroscience – Page 218

Frontiers: Brain organoids have become increasingly used systems allowing 3D-modeling of human brain development, evolution, and disease

To be able to make full use of these modeling systems, researchers have developed a growing toolkit of genetic modification techniques. These techniques can be applied to mature brain organoids or to the preceding embryoid bodies (EBs) and founding cells. This review will describe techniques used for transient and stable genetic modification of brain organoids and discuss their current use and respective advantages and disadvantages. Transient approaches include adeno-associated virus (AAV) and electroporation-based techniques, whereas stable genetic modification approaches make use of lentivirus (including viral stamping), transposon and CRISPR/Cas9 systems. Finally, an outlook as to likely future developments and applications regarding genetic modifications of brain organoids will be presented.

The development of brain organoids (Kadoshima et al., 2013; Lancaster et al., 2013) has opened up new ways to study brain development and evolution as well as neurodevelopmental disorders. Brain organoids are multicellular 3D structures that mimic certain aspects of the cytoarchitecture and cell-type composition of certain brain regions over a particular developmental time window (Heide et al., 2018). These structures are generated by differentiation of induced pluripotent stem cells (iPSCs) or embryonic stem cells (ESCs) into embryoid bodies followed by, or combined, with neural induction (Kadoshima et al., 2013; Lancaster et al., 2013). In principle, two different classes of brain organoid protocols can be distinguished, namely: (i) the self-patterning protocols which produce whole-brain organoids; and (ii) the pre-patterning protocols which produce brain region-specific organoids (Heide et al., 2018).

Brain prosthesis passes live tissue test

The world’s first brain prosthesis has passed the first stages of live testing.

The microchip, designed to model a part of the brain called the hippocampus, has been used successfully to replace a neural circuit in slices of rat brain tissue kept alive in a dish. The prosthesis will soon be ready for testing in animals.

The device could ultimately be used to replace damaged brain tissue which may have been destroyed in an accident, during a stroke, or by neurodegenerative conditions such as Alzheimer’s disease. It is the first attempt to replace central brain regions dealing with cognitive functions such as learning or speech.

A hippocampal circuit mechanism to balance memory reactivation during sleep

Memory consolidation involves the synchronous reactivation of hippocampal cells active during recent experience in sleep sharp-wave ripples (SWRs). How this increase in firing rates and synchrony after learning is counterbalanced to preserve network stability is not understood. We discovered a network event generated by an intrahippocampal circuit formed by a subset of CA2 pyramidal cells to cholecystokinin-expressing (CCK+) basket cells, which fire a barrage of action potentials (“BARR”) during non–rapid eye movement sleep. CA1 neurons and assemblies that increased their activity during learning were reactivated during SWRs but inhibited during BARRs. The initial increase in reactivation during SWRs returned to baseline through sleep. This trend was abolished by silencing CCK+ basket cells during BARRs, resulting in higher synchrony of CA1 assemblies and impaired memory consolidation.

Miller School Scientists Reveal Mechanisms Behind Gene Expression in Mitochondria

A molecular biology research team at the University of Miami Miller School of Medicine has become the first to map out how mitochondrial messenger RNA folds in human cells.

The research advances knowledge about the expression of genes in the mitochondria and paves the way for identification of therapeutic targets for mitochondrial neurodegenerative diseases.

“Dysfunctional mitochondria can cause devastating diseases, frequently with childhood-onset, known as mitochondrial encephalomyopathies. Despite advances in identifying genes responsible for these disorders, their pathophysiological mechanisms have been poorly understood,” said Antoni Barrientos, Ph.D., professor of neurology and biochemistry and molecular biology at the Miller School. “This was partly due to a lack of a full understanding of mitochondrial gene expression. Specifically, nothing was known about how mitochondrial messenger RNA folds and how that could influence its stability and translation in health and disease.”

The Shape of the Brain: Spatial Biology of Alzheimer’s Disease

Using #CellDIVE multiplexed imaging and antibodies from Cell Signaling Technology to uncover cell identity and brain structure in Alzheimer’s disease, demonstrating how spatial biology can lead to advances in therapy development for neuro degeneration.

🖼️: Adult Human Alzheimer’s brain demonstrating a panel of 15 markers.

Uncover cell identity and brain structure in Alzheimer’s disease with Cell DIVE multiplexed imaging, demonstrating how spatial biology can lead to advances in therapy development for neurodegeneration.

Stanford Reverses Cognitive Decline in Alzheimer’s With Brain Metabolism Drug

Neuroscientists at Stanford have linked Alzheimer’s disease to the disruption of brain metabolism via the kynurenine pathway, which is affected by amyloid plaque and tau proteins.

Their research has demonstrated that drugs blocking this pathway can restore cognitive function in Alzheimer’s mice by improving brain metabolism. This discovery not only bridges the gap between neuroscience and oncology but also provides a fast track to repurposing existing drugs for Alzheimer’s treatment.

Alzheimer’s disease and brain energy metabolism.

Brain Overgrowth Linked to Autism Symptom Severity

Summary: Researchers have identified a link between brain overgrowth and the severity of social and communication symptoms in children with autism spectrum disorder (ASD).

By analyzing MRI scans and conducting experiments with brain organoids, the study found that children with the most severe ASD symptoms had significantly larger brains. This enlargement is associated with altered activity of the enzyme Ndel1, which plays a crucial role in neuron development.

The findings open new avenues for understanding ASD and its varying symptom severity.