Dietmar Rudolf Thal

The paper analyzes somatic mutations in neurons from FTLD-TDP type C patients and controls, finding extensive low-frequency variants in TARDBP and other genes.

The paper creates a single-nucleus transcriptomic atlas of oligodendrocytes in ALS, identifying disease-associated activation states and potential biomarkers.

This study shows human macrophages and microglia actively produce Aβ42 fibrils, which seed amyloid plaques and tau aggregation, and this process is influenced by genetic factors like TREM2.

This study shows 4'-fluorouridine inhibits Oropouche virus replication in vitro and in animal models, with no resistant variants observed.

This study examines the interactions between A{beta}, tau, LATE-NC, -synuclein, and APOE {varepsilon}4 in 480 post-mortem brains, finding that tau is the strongest predictor of neurodegeneration while LATE-NC primarily affects hippocampal neuron loss.

This study shows that pathological tau spreads from the olfactory epithelium to brain regions in AD models and suggests targeting the olfactory epithelium to slow tauopathy progression.

This study shows that amygdala-predominant α-synuclein pathology is linked to reduced hippocampal neuron density in Alzheimer's disease, mediated through pTau and LATE-NC.

The paper analyzes single-cell transcriptomics data from Parkinson's Disease patients and controls to identify cell type-specific molecular responses and pathways involved in neurodegeneration.

This study shows that C9orf72 hexanucleotide repeat expansions impair microglial function and disrupt glial communication in ALS, contributing to disease risk.

The paper shows that astrocyte calcium dysfunction leads to early network hyperactivity in Alzheimer's Disease, which can be reversed by restoring calcium signaling.

The paper shows that MEG3, a long noncoding RNA, induces necroptosis in human neurons exposed to amyloid pathology, mimicking AD features in a xenograft model.

The paper transplants human iPSC-derived astrocytes into mouse brains to study their response to amyloid-β plaques, finding morphological changes independent of APOE alleles.

This study identifies impaired MCH-system function in AD models and patients, disrupting synaptic downscaling and neuronal activity stability.

This study shows that C9orf72 repeat expansions produce toxic arginine-rich DPRs that disrupt axonal transport by interacting with microtubules and motor proteins, contributing to ALS/FTD.

This study identifies miR-132 deficiency as a cause of impaired adult hippocampal neurogenesis in Alzheimer's disease and shows that restoring miR-132 levels can reverse these deficits and memory issues.