Adam Bachstetter
@bachstetterlab.bsky.social
220 followers 210 following 8 posts
Associate Professor, Dept. of Neuroscience, SCoBIRC, Sander-Brown Center on Aging, University of Kentucky | passions = glia, TBI, aging, and Alzheimer's disease / ADRD
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Reposted by Adam Bachstetter
bachstetterlab.bsky.social
Rising Star at #KSCHIRT: Dr. Catie Profaci (@cprofaci.bsky.social), postdoc in the Patapoutian Lab (@ardemp.bskyverified.social), delivered a standout talk on PIEZO1 mechanosensation in the choroid plexus. Grateful for her visit to Kentucky—excited to follow the work of a true star on the rise!
Reposted by Adam Bachstetter
aosasmita.bsky.social
Are you using 5xFAD mice to study Alzheimer’s disease? Our work out today @cp-neuron.bsky.social may be relevant to you 🐁🧠 Age and sex are known to influence Aβ plaque burden in these mice. Here, we found that the transgene parentage is another strong determinant.

Thread below: (1/11)
Parental origin of transgene modulates amyloid-β plaque burden in the 5xFAD mouse model of Alzheimer’s disease
The 5xFAD transgenic model, popular in Alzheimer’s disease research, exhibits varying cerebral plaque burden depending on the parental source of the transgene. Mice inheriting the transgene paternally...
www.cell.com
Reposted by Adam Bachstetter
nfranzme.bsky.social
Very happy to share the first PhD work by Hannah de Bruin, showing that traumatic brain injury is not linked to higher fibrillar amyloid and tau per se, but to altered patterns of tau deposition preferentially in TBI vulnerable regions
doi.org/10.1093/brai...
@rikossenkoppele.bsky.social
Amyloid-β and tau deposition in traumatic brain injury: a study of Vietnam War veterans
De Bruin et al. report that traumatic brain injury does not inherently elevate the Alzheimer’s pathologies amyloid-β or tau, but is associated with their u
doi.org
Reposted by Adam Bachstetter
johnsonlab.bsky.social
new preprint!

www.biorxiv.org/content/10.1...

a characterization of APOE effects on the lipid droplet-ome (turns out you see a lot of "AD-related" proteins!)

first authors Cassi Friday & Isaiah Stephens + great collaborators Scott Gordon, @cohenlaboratory.bsky.social @morganti.bsky.social
bachstetterlab.bsky.social
Simic et al. engineered T cells with synthetic receptors to target brain-localized antigens, activating circuits to kill cancer cells specifically in the brain. Could this precision pave the way for T cell therapies in neurodegenerative diseases?

doi.org/10.1126/scie...
Programming tissue-sensing T cells that deliver therapies to the brain
To engineer cells that can specifically target the central nervous system (CNS), we identified extracellular CNS-specific antigens, including components of the CNS extracellular matrix and surface mol...
doi.org
bachstetterlab.bsky.social
Glögl et al. used AI-driven protein design (RFdiffusion) to create selective antagonists for TNFR1, a pro-inflammatory TNF receptor, without targeting the anti-inflammatory TNFR2. This shows the potential of AI tools in therapeutic protein design.

doi.org/10.1126/scie...
Target-conditioned diffusion generates potent TNFR superfamily antagonists and agonists
Despite progress in designing protein-binding proteins, the shape matching of designs to targets is lower than in many native protein complexes, and design efforts have failed for the tumor necrosis f...
doi.org
bachstetterlab.bsky.social
Congratulations to Lance Johnson on his excellent talk at the CSHL Neurodegenerative Disease conference on his ApoE switch mice. In my (biased) opinion, it sparked some of the most interesting questions of the meeting!
bachstetterlab.bsky.social
Zhuang et al. show that aging alters iron handling and ferroptosis. Aged cells resist ferroptosis due to reduced iron levels, while young cells rely on iron to maintain stemness. This raises interesting questions about aging and iron regulation in other cell types.

doi.org/10.1038/s415...
Ageing limits stemness and tumorigenesis by reprogramming iron homeostasis - Nature
Studies using mouse models of lung adenocarcinoma identify an association between age, iron homeostasis and tumour initiation potential that involves NUPR1 and lipocalin-2.
doi.org