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A novel regulatory cascade downstream of Tau and spectraplakins ensures that synaptic proteins are delivered to axonal terminals in the developing and ageing brain, providing potential explanations for precocious synapse loss in dementias.

Alteration of the G-quadruplex structure formed by GGGGCC repeat RNA through the direct interaction with RNA-binding proteins can suppress pathogenic repeat-associated non-AUG translation, leading to therapeutic effects on neurodegeneration in C9orf72-linked amyotrophic lateral sclerosis and frontotemporal dementia.

A traumatic brain injury model is invented for larval zebrafish and applied to a new fluorescent 'tauopathy reporter fish', revealing a role for seizures in progression towards dementias.

The Wnt antagonist DKK3 is a key regulator of excitatory and inhibitory synapses, and its downregulation in the hippocampus restores synaptic connectivity and memory in an Alzheimer's disease mouse model.

Proteins implicated in Alzheimer’s disease, including amyloid precursor protein and ApoE receptors, interact with each other and with a signalling molecule called agrin to influence the development of the neuromuscular junction.

APP mutations that either cause or prevent dementia alter APP metabolism in a complex and opposite fashion, suggesting a link between multiple APP processing events, dementia and ageing-dependent cognitive decline.

Length-dependent interference of arginine-containing dipeptide repeat proteins with multiple components of the nucleocytoplasmic transport machinery is a potential mechanistic pathway of C9orf72 amyotrophic lateral sclerosis or frontotemporal dementia toxicity.

Convergent screens targeting the levels of alpha-synuclein and tau identify TRIM28 as a driver of their stability, nuclear accumulation and subsequent toxicity.

OptoGranules reveal the function of G3BP1 as a stress granule scaffold and demonstrate that protracted stress granule assembly is sufficient to drive neurodegeneration and the evolution of ALS-FTD pathology.

While tau and aging have highly overlapping differential gene expression signatures, they diverge in the affected cell types, with aging having a wide-ranging impact and tau-triggered changes instead polarized to excitatory neurons and glia.