Scientists from the UK Dementia Research Institute at the University of Cambridge have described how cytosolic antibody receptor TRIM21 contributes to in vivo protection during tau immunotherapy. Their work on TRIM21’s mechanism of action may help in moving a step closer toward enhanced second-generation antibodies for tauopathy treatments.

Losing the tail to survive. In neurons, the lizard’s strategy, losing the axon to be safe, could prevent cell death. Scientists at Harvard Medical School have observed that certain toxins activated axon loss to prevent damage and survive. This mechanism was mediated by the Gasdermin-E (GSDME) protein, which destroyed the mitochondria in the axons and eliminated the affected nerve projection before the cell died. The inhibition of GSDME prevented the loss of neurons and delayed the progression of amyotrophic lateral sclerosis (ALS) in mice models.

Scientists from Washington University in St. Louis have described a role for T cells in the neurodegeneration associated with the tau protein. Tau accumulation in the brain activated microglia. This signal triggered the activation of T cells in other parts of the body, attracting them to the brain. Once there, the interaction of these T cells and microglia produced the neuronal damage seen in Alzheimer’s disease and other tauopathies.

Microglial cells (MGs) are resident immune cells in the brain, which play a key role in the acute response and chronic recovery to stroke. Investigators at the University of Texas Health Science Center Houston aimed to evaluate MG transcriptomic response to stroke in mouse brain.

Fundamental Pharma GmbH has raised €10 million (US$10.3 million) in a seed round to develop a new class of glutamate inhibitors, after uncovering a route to maintaining the protective effects of the neurotransmitter in the synapses while preventing neurotoxicity when it is released elsewhere.

The mutant gene causing Huntington’s disease (HD) is active from the earliest stages of brain development, even though the pathology is not evident until between 30 and 50 years of age. That delay is ascribed to plasticity enabling the brain to compensate to such an extent that overt signs of disease take time to develop. As a result, it is difficult to plot a route from early molecular defects to development of HD several decades later.

Age-related diseases have been explained as due in part to the excessive generation and accumulation of waste products like the various insoluble protein aggregates observed in nondividing neurons of Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis and Huntington’s disease.

Connections, Susan Greenfield told her audience at the 2022 Annual Conference of the European Academy of Neurology, are what the mind is all about. "When you are born, you are born with a fair amount of neurons," she said at the conference's opening plenary on Sunday. But "what characterizes the growth of the brain postnatally is the configurations of connections."

Researchers report in the June 21, 2021, online issue of Neuron that overexpression of the LDL receptor can reduce ApoE to prevent tauopathy-associated neurodegeneration in mouse models.