The evidence presented by Boldrini et al² was considered resilient and convincing because the authors ensured that the samples were taken from healthy individuals using more biological parameters, such as angiogenesis and change in volume of DG, for a suitable comparison. They also employed unbiased stereology, which is the gold standard for counting number of neurons.²

The contrary results presented by the Sorrels study and Boldrini study highlight the existing ambiguity regarding the concept of neurogenesis in adult humans. Both studies employed reasonably similar immunohistological methods and included many of the same neurogenesis markers, yet contrasting results were observed. The study by Boldrini et al examined samples from humans aged 14 to 79 years, finding more than a thousand cells in each part of the DG, which was in stark contrast to what was observed by Sorrells et al, who found very few cells in the neurogenic niche of subjects in the same age range. Even if we consider that some discrepancies in numbers might arise due to the difference in counting methods (or subjective reasons), such marked and obvious disparity is perplexing. Sorrels et al justified their findings, noting the limitation that relying solely on the presence of markers might cause glial lineage cells to be identified as neuronal lineage cells. However, the authors stated that they used additional methods for confirmation, including transmission electron microscopy (TEM)-immunogold and in-situ hybridization. The relative paucity of any type of progenitor or immature cells, including glia in the neurogenic niche of DG in their study, remains unexplained.

Kempermann et al⁷ expressed skepticism regarding the negative findings of Sorrells et al, naming the postmortem interval, the lack of known status regarding neuropsychiatric disease or chronic ailment, and using patients with epilepsy as key factors of concern.⁷ Kempermann et al argued that, in severe epilepsy, destruction of the neurogenic niche is an explicit possibility, and that, in some cases, epilepsy could be the reason for the lack of neurogenesis.⁷ Additionally, Kempermann et al also criticized the use of 10% formalin in some of the samples due its potential to mask the expression of proteins.⁷ However, Sorrells et al clearly mentioned that they performed appropriate antigen retrieval for the selected sections.¹ Kempermann et al⁷ suggested that dependence on the protein markers to denote neurogenesis could be an erroneous approach and that some of the markers, such as DCX, are known for fast degradation. Additionally, the presence of DCX-negative immature neurons and high inter-individual variation in expression of DCX in humans, which was also reflected in the data presented by Boldrini et al, are not unusual.⁷ The use of fluorescence markers also was presented as a caveat by Kempermann et al⁷ because it is prone to fade away and might give rise to false negative impression.

Monitoring electrical signals in biological systems helps scientists understand how cells communicate, which can aid in the diagnosis and treatment of conditions like arrhythmia and Alzheimer’s.

But devices that record electrical signals in cell cultures and other liquid environments often use wires to connect each electrode on the device to its respective amplifier. Because only so many wires can be connected to the device, this restricts the number of recording sites, limiting the information that can be collected from cells.

MIT researchers have now developed a biosensing technique that eliminates the need for wires. Instead, tiny, wireless antennas use light to detect minute electrical signals.

The standard medication levodopa does not always work against tremors in Parkinson’s disease, especially in stressful situations. Propranolol, however, does work during stress, providing insight into the role of the stress system in tremors. MRI scans reveal that propranolol directly inhibits activity in the brain circuit that controls tremors. Doctors may consider this medication when levodopa is ineffective.

People with Parkinson’s disease report that tremors worsen during stressful situations. “Tremors act as a sort of barometer for stress; you see this in all people with Parkinson’s,” says neurologist Rick Helmich from Radboud university medical center.

The commonly used drug levodopa usually helps with tremors, but it tends to be less effective during stress, when tremors are often at their worst. Helmich and his team wanted to investigate whether a medication targeting the stress system could help and how this effect of stress on tremors works in the brain. The work is published in the journal Annals of Neurology.

Researchers from Helmholtz Munich and Ludwig-Maximilians-Universität (LMU) have identified a mechanism that may explain the neurological symptoms of long COVID.

The study shows that the SARS-CoV-2 spike protein remains in the brain’s protective layers, the meninges, and the skull’s bone marrow for up to four years after infection. This persistent presence of the spike protein could trigger chronic inflammation in affected individuals and increase the risk of neurodegenerative diseases.

The team, led by Prof. Ali Ertürk, Director at the Institute for Intelligent Biotechnologies at Helmholtz Munich, also found that mRNA COVID-19 vaccines significantly reduce the accumulation of the spike protein in the brain. However, the persistence of spike protein after infection in the skull and meninges offers a target for new therapeutic strategies.