Celeste M M. Karch

This study identifies TMEM106B as an alternative receptor for SARS-CoV-2 S-E484D variant entry, independent of ACE2, in airway-derived cell models.

This study shows that C4 deficiency reduces amyloid plaques and neuroinflammation in a mouse AD model, suggesting C4's role in glial reactivity and pathology.

This study shows that pathogenic MAPT mutations impair microglial lysosomal and autophagic functions, affecting tau clearance and degradative capacity.

This study shows that loss of Ms4a4a remodels microglial transcriptional programs and reduces dense-core plaque-associated tau spreading in a mouse model of Alzheimer's disease.

The paper characterizes big tau isoforms in human nervous system tissues and CSF, finding they are enriched in the peripheral nervous system and largely unaffected by neurodegenerative disease.

This study evaluates how biomarker variability affects individualized amyloid time estimation in Alzheimer's disease, finding that inter-individual variability is the main source of error.

The paper identifies lncRNA dysregulation in MAPT mutation carriers and shows the NORAD-pumilio axis modulates tau propagation.

The paper characterizes 85 MAPT mutation-bearing iPSC lines using multiomic approaches, revealing cellular diversity and factors influencing organoid development.

The paper identifies NINL as a modulator of tau aggregation through integrative genomic and functional analyses linking it to proteostasis dysfunction in FTD and AD.

This paper describes a reproducible method to generate rhesus macaque induced pluripotent stem cells (RhiPSCs) from MAPT R406W carriers for in vitro modeling of frontotemporal dementia.

This study shows that Ms4a4a deficiency reduces amyloid beta pathology in mice by enhancing Aβ clearance, supported by increased MMP-9 production in microglia and human CSF data.

The paper investigates cell-to-cell communication in Alzheimer's disease to characterize disease biology and suggest new avenues for therapeutic intervention.

This study shows that a mutation in the MAPT gene disrupts autophagy in neurons, leading to Tau accumulation, and that an autophagy enhancer drug reduces Tau levels.

This study uses 3D direct neuronal reprogramming of AD patient fibroblasts to recapitulate AD neuropathology, showing A{beta} deposition, tauopathy, and neuronal death, and identifies potential therapeutic targets.

The paper develops fully human bifunctional anti-tau intrabodies that reduce intracellular tau and improve neuronal survival in disease-associated mutations.

The paper identifies m6A-dependent circRNA dysregulation as a causal factor in tau-induced neurotoxicity using Drosophila and iPSC models.

This study shows hub disruption in ADAD follows a targeted attack pattern, detectable pre-clinically and linked to amyloid beta changes and neuronal activity.

The paper develops a scalable cortical organoid platform with quality control metrics and identifies early dysregulation of phosphatase and prefoldin genes in FTD-tau neurons.

The paper quantifies Aβ production from PSEN1 variants and links it to clinical and biomarker progression in ADAD, showing strong associations with disease trajectories.

The paper integrates multi-omics data from Alzheimer's disease cohorts to identify molecular profiles linked to disease progression and severity.

This study identifies estrogen's role in suppressing neuro-inflammation and links its loss to increased Alzheimer's disease risk in women through systems pharmacology and signaling network analysis.

The paper identifies three H1 sub-haplotypes at the 17q21.31 locus associated with Parkinson's disease risk and links them to LRRC37A/2 expression in astrocytes.

The paper describes MRI and PET protocols used in the DIAN study to investigate preclinical Alzheimer's disease and reports key imaging findings.

This study shows that Kir6.2-KATP channels are necessary for hyperglycemia-induced increases in amyloid-beta and Alzheimer's pathology by regulating lactate transport and Aβ release.

This study shows that caspase inhibition reduces tau cleavage and neurotoxicity in iPSC-derived neurons with the V337M MAPT mutation.

This study identifies metabolomic and lipidomic signatures in Alzheimer's disease brains with different genetic risk factors and finds associations with disease subtypes and progression.

This study shows human brain organoids can form bilateral optic vesicles with cellular diversity and functionality, including light-responsive photoreceptors and neuronal networks.