@northernthrux.bsky.social with a timely Feindel lecture opening! #gohabsgo
Neuromodulatory neurons are extremely susceptible to stress. I argue that their fragility is an inherent weak point, the breaking of which directly leads to Alzheimer’s Disease.
I discuss this idea and its implications in a recently published perspective piece:
dx.doi.org/10.1002/alz....
We first propose that innate morphofunctional BFCN vulnerabilities, established in both evolution and development, interact with midlife stressors to trigger a cascade of events that contribute to BFCN dysfunction and degeneration. (2/4)
Hot off the press Huge congrats to Alycia Crook a PhD student from the lab www.nature.com/articles/s41...
Sporadic Alzheimer's disease (AD) is associated with numerous risk factors, yet its precise cause remains unclear. Here, we describe a novel framework for AD pathogenesis, whereby diverse risk factor...
This study uses a transgenic mouse line expressing Cre-inducible astro-hM3Dq to study astrocytes’ role in neuroinflammation and cognition without the use of viral transduction, mitigating the potentia...
Finally, we articulate an urgent and unmet need for in vivo cholinergic biomarkers to deepen our knowledge of the timing and progression of BFCN dysfunction. Understanding such events will be critical for identifying new avenues for therapeutic development. (4/4)
fire away @kateonuska.bsky.social #adpd2026
Latest paper is Vlad Novikov’s careful analysis of proteostasis in a TDP-43 mouse model
A Longitudinal Study of Sex Differences in a TDP‐43 Mouse Model Reveals STI1 Regulation of TDP‐43 Proteinopathy and Motor Deficits - Journal of Neurochemistry - onlinelibrary.wiley.com/doi/10.1111/...
Grad student extraordinaire @kateonuska.bsky.social dropped this preprint www.biorxiv.org/content/10.1... using
multimodal imaging, behavior, 🐁 and human datasets to show how cholinergic plasticity regulates resilience to Alzheimer’s pathology. Led by Taylor Schmitz 🧪
We then review existing evidence suggesting that the heightened vulnerability of BFCNs further aggravates the progression of Aβ, tau, and neuroinflammatory species, contributing to the spread of pathophysiological signatures to functionally and anatomically connected brain regions. (3/4)
