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Experiment #00000126

Hypothesis: Intranasal delivery of Spermidine-modified Ginseng Extracellular Vesicles (S-GEVs) loaded with multi-targeted mRNA suppresses MARK2-eIF2α-driven RAN translation to prevent dipeptide repeat clogging of FG-nucleoporins, synergizing with progranulin-mediated lysosomal clearance to arrest TMEM106B amyloid accumulation and block the execution of p38-Lamin B1-dependent Karyoptosis in motor neurons.

Spermidine _gates_from_spermidine Lysosomal Degradation _gates_to_lysosomal_degradation _gates_from_lysosomal_degradation Protein Aggregates _gates_to_protein_aggregates _gates_from_protein_aggregates Cell Death _gates_to_cell_death
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Experiment #00000125

Discovery: Considering PubMed #37563705, #42012729, and #42541426, Spermidine is a known inducer of autophagy through EP300 inhibition and TFEB activation. Since TMEM106B amylofilaments induce lysosomal dysfunction, TFEB-driven restoration of lysosomal capacity would logically prevent the accumulation of these filaments.

Spermidine _gates_from_spermidine Transcription Factor EB _gates_to_transcription_factor_eb _gates_from_transcription_factor_eb Lysosomes _gates_to_lysosomes _gates_from_lysosomes TMEM106B protein _gates_to_tmem106b_protein
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Experiment #00000124

Hypothesis: Intranasal delivery of Spermidine-modified Ginseng Extracellular Vesicles (S-GEVs) loaded with GRN mRNA exploits the cribriform plate anatomy to bypass the blood-brain barrier, providing a neuro-targeted delivery system for progranulin gene therapy that acts synergistically with spermidine-induced autophagy to suppress pathological TMEM106B amyloid accumulation and restore endolysosomal homeostasis.

Administration, Intranasal _gates_from_administration__intranasal Olfactory Bulb _gates_to_olfactory_bulb Progranulins _gates_from_progranulins _gates_to_progranulins RNA, Messenger _gates_from_rna__messenger PGRN protein
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Experiment #00000123

Hypothesis: Intranasal delivery of Spermidine-modified Ginseng Extracellular Vesicles (S-GEVs) loaded with GRN mRNA exploits the cribriform plate anatomy to bypass the blood-brain barrier, providing a neuro-targeted delivery system for progranulin gene therapy that acts synergistically with spermidine-induced autophagy to suppress pathological TMEM106B amyloid accumulation and restore endolysosomal homeostasis.

Administration, Intranasal _gates_from_administration__intranasal Olfactory Bulb _gates_to_olfactory_bulb Progranulins _gates_from_progranulins _gates_to_progranulins RNA, Messenger _gates_from_rna__messenger PGRN protein
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Experiment #00000050

What are the symptoms of toxoplasmosis and how is it transmitted?

Host _gates_from_host Infection _gates_to_infection _gates_from_infection Clinical Symptoms _gates_to_clinical_symptoms Animals, Domestic _gates_from_animals__domestic Environment
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Experiment #00000049

Explain the risks of veridical AI and human job displacement.

Artificial Intelligence _gates_from_artificial_intelligence Efficiency, Organizational _gates_to_efficiency__organizational _gates_from_efficiency__organizational Employment _gates_to_employment _gates_from_employment Patient-Centered Care _gates_to_patient_centered_care
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Experiment #00000042

#PITRM1 #ALS #Microglia #Mitochondria

PITRM1 protein, human _gates_from_pitrm1_protein__human Unfolded Protein Response _gates_to_unfolded_protein_response Mitochondrial Stress _gates_from_mitochondrial_stress DNA, Mitochondrial _gates_to_dna__mitochondrial _gates_from_dna__mitochondrial Neuroinflammation
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Experiment #00000016

Analyze the potential for zinc-binding competition between synaptic transporters (e.g., SLC39A8, ZnT3) and ALS-associated proteins (RGNEF, TDP-43) in the RGC-thalamic axis. Can this competition explain the coexistence of RGC excitotoxicity and STMN2 depletion in clinical samples?

TAR DNA-Binding Protein 43 _gates_from_tar_dna_binding_protein_43 Stathmin 2 _gates_to_stathmin_2 SLC39A8 protein, human _gates_from_slc39a8_protein__human Zinc _gates_to_zinc Excitotoxicity _gates_from_excitotoxicity
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Experiment #00000007

Simply put, we still don’t know why neurons are dying in ALS, and why motor neurons die while other types of neurons don’t. Even for genetic forms c9orf72 familial ALS, why is it that the mutation is in every cell but the motor neurons are dying ie have increased susceptibility?

Axonal Transport _gates_from_axonal_transport Motor Neuron Disease _gates_to_motor_neuron_disease C9orf72 Repeat Expansion _gates_from_c9orf72_repeat_expansion Dipeptide Repeats _gates_to_dipeptide_repeats _gates_from_dipeptide_repeats VAPB protein, human
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