Distinct Effects of Aging and Klotho Deletion on the Choroid Plexus
Fanaei-Kahrani, Z.; Patel, T.; Valkova, C.; Gloria, A.; Wagner, J.; Heuer, H.; Schwaninger, M.; Hoffmann, S.; Bauer, R.; Kaether, C.
Show abstract
Klotho (Kl) is an anti-aging protein primarily produced in the kidney and the choroid plexus (CP, where it regulates cerebrospinal fluid composition and exerts neuroprotective effects. Here, we investigated the age-dependent consequences of a CP-specific Kl deletion on CP structure and function using mice lacking KL exclusively in CP epithelial cells (Kl{Delta}CP). In control mice, aging markedly disrupted CP architecture and cilia organization both in the lateral (LV-CP) and fourth ventricle (FV-CP). While CP-specific Kl deletion alone caused no major structural changes it induced region- and age-dependent calcification: FV-CP calcification increased in both aged and young Kl{Delta}CP mice, whereas LV-CP calcification emerged only in older Kl{Delta}CP mice. Proteomic analysis of the CP and hippocampus revealed mild molecular alterations, suggesting compensatory mechanisms that preserve structural and functional stability despite calcium dysregulation. Consistently, Kl{Delta}CP mice exhibited no significant behavioral or cognitive deficits. Overall, Kl deficiency sensitizes the CP to age-related calcification prior to overt structural decline, revealing a region-specific and functional link between Klotho, calcium imbalance, and brain aging.
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Muscle Cathepsin B treatment improves behavioral and neurogenic deficits in a mouse model of Alzheimer's Disease 95%
- Canagliflozin reprograms the aging hippocampus in genetically diverse UM-HET3 mice and attenuates Alzheimer's-like pathology 95%
- A scalable organoid model of urothelial aging for metabolic interrogation, infection modeling, and reversal of age-associated changes 95%
Similar papers in this journal
- Necroptosis increases with age in the brain and contributes to age-related neuroinflammation 97%
- Cross-platform proteomics signatures of extreme old age 95%
- Activation of the muscle-to-brain axis ameliorates neurocognitive deficits in an Alzheimer disease mouse model via enhancing neurotrophic and synaptic signaling 95%
Similar papers in this journal
Similar papers in this journal
- Proteomic and transcriptomic profiling reveal different aspects of aging in the kidney 96%
- Aging is associated with increased brain iron through brain-derived hepcidin expression 94%
- Scleraxis-lineage cells are required for tendon homeostasis and their depletion induces an accelerated extracellular matrix aging phenotype 94%
Similar papers in this journal
- Plcg2M28L interacts with high fat-high sugar diet to accelerate Alzheimers disease-relevant phenotypes in mice 95%
- Dual-specificity protein phosphatase 6 (DUSP6) overexpression reduces amyloid load and improves memory deficits in male 5xFAD mice 95%
- Shifted dynamics of glucose metabolism in the hippocampus during aging 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.