Search Results for "autophagy"

Experiment #00000139

Foundational Dietary Theory: The dietary synergy between Hi-Maize and 6x Spermidine Yeast creates a potential cellular supply-and-clearance loop within the brain's astrocytes. Circulating spermidine metabolites utilize documented astrocytic polyamine uptake systems to access the central nervous system. Once inside, this exogenous spermidine drives FAM134B-mediated ER-phagy, clearing the endoplasmic reticulum matrix. This clearance removes the ER-stress bottleneck, allowing newly transcribed astrocytic EAAT2—upregulated by gut-derived butyrate from Hi-Maize fermentation—to successfully traffic to the plasma membrane and mitigate synaptic glutamate excitotoxicity.

Starch, Resistant _gates_from_starch__resistant Butyric Acid _gates_to_butyric_acid _gates_from_butyric_acid Glutamate Plasma Membrane Transport Proteins _gates_to_glutamate_plasma_membrane_transport_proteins Spermidine _gates_from_spermidine Autophagy

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Experiment #00000128

Discovered Hypothesis: Spermidine-mediated autophagic activation may serve as an upstream regulator of lysosomal TMEM175 activity to prevent proteinopathy in C9orf72-ALS/FTD models.

Spermidine _gates_from_spermidine Autophagy _gates_to_autophagy _gates_from_autophagy Lysosomal Integrity _gates_to_lysosomal_integrity _gates_from_lysosomal_integrity TMEM175 _gates_to_tmem175

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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 #00000116

How do electrophilic binding and charge polarity modulate proteinopathy in Alzheimer's Disease, specifically regarding BBB interactions?

Metabolic State _gates_from_metabolic_state βHB Production _gates_to___hb_production 3-Hydroxybutyric Acid _gates_from_3_hydroxybutyric_acid Protein Aggregates _gates_to_protein_aggregates _gates_from_protein_aggregates Autophagy

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Experiment #00000115

Ebola Virus Outbreak Solution Hypothesis: Oral ginger-derived extracellular vesicles may serve as an acid-stable, inexpensive, and supply-chain ready clinical solution to deliver 6-shogaol to macrophages, triggering CASA autophagy to degrade EBOV VP40 and halt viral egress.

Ginger extract _gates_from_ginger_extract Autophagy _gates_to_autophagy Autophagy (CASA) _gates_from_autophagy__casa_ Viral Matrix Proteins _gates_to_viral_matrix_proteins Proteolysis _gates_from_proteolysis

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Experiment #00000105

Gap Analysis: There is no PubMed data showing wet lab data or analysis of TPD-43 proteinopathy found (or not found) in the Cochlear, Spiral, or Scarpa's Ganglion of Amyotrophic Lateral Sclerosis patient data post mortem.

Amyotrophic Lateral Sclerosis _gates_from_amyotrophic_lateral_sclerosis TDP-43 proteinopathy _gates_to_tdp_43_proteinopathy _gates_from_tdp_43_proteinopathy Spiral Ganglion _gates_to_spiral_ganglion Peripheral Nerves _gates_from_peripheral_nerves _gates_to_amyotrophic_lateral_sclerosis

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Experiment #00000086

Parkinson's Disease versus Alzheimer's Disease: Shared and Exclusive Pathways

Pathologic Processes _gates_from_pathologic_processes Mitochondrial Diseases _gates_to_mitochondrial_diseases Lipid Metabolism Disorders _gates_from_lipid_metabolism_disorders Lipid Droplet Accumulation _gates_to_lipid_droplet_accumulation _gates_from_lipid_droplet_accumulation Lysosomal Storage Diseases

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Experiment #00000077

The use of lysosome-acidifying nanoparticles (AcNPs) could potentially be adapted to treat nanoplastic-induced lysosomal alkalization or membrane rigidification, as these nanoparticles act to restore the degradative capacity lost during environmental contaminant stress.

Nanoplastic exposure _gates_from_nanoplastic_exposure Lysosomes _gates_to_lysosomes _gates_from_lysosomes Autophagy _gates_to_autophagy Nanoparticles _gates_from_nanoparticles Hydrogen-Ion Concentration

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Experiment #00000074

OGT (O-GlcNAc transferase) modulation via pharmacological agonists can prevent degeneration of cranial nerves following traumatic or surgical stress.

Trauma/Stress _gates_from_trauma_stress Ferritinophagy/Oxidative Stress _gates_to_ferritinophagy_oxidative_stress Autophagy _gates_from_autophagy N-Acetylglucosaminyltransferases _gates_to_n_acetylglucosaminyltransferases _gates_from_n_acetylglucosaminyltransferases Neuronal Survival

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Experiment #00000036

What is Karyoptosis and how does it align with past and present neurodegenerative disease research? Does Karyoptosis provide a new context in which a new class of repurposed therapeutics is formed?

Proteotoxic Stress _gates_from_proteotoxic_stress Cyclic AMP-Response Element Binding Protein _gates_to_cyclic_amp_response_element_binding_protein _gates_from_cyclic_amp_response_element_binding_protein Nuclear Envelope _gates_to_nuclear_envelope _gates_from_nuclear_envelope Apoptosis _gates_to_apoptosis

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Experiment #00000009

How does autophagy work?

Cellular Stress _gates_from_cellular_stress Autophagy _gates_to_autophagy _gates_from_autophagy Phagosomes _gates_to_phagosomes _gates_from_phagosomes Apoptosis _gates_to_apoptosis

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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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Experiment #00000006

Does existing in vitro data show that Quercetin-induced autophagy can successfully degrade DUX4 or its downstream misfolded proteins?

Quercetin _gates_from_quercetin Autophagy _gates_to_autophagy _gates_from_autophagy Misfolded Proteins _gates_to_misfolded_proteins _gates_from_misfolded_proteins DUX4 _gates_to_dux4

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Experiment #00000003

Does long-term microplastic or bisphenol exposure act as a catalyst for alpha-synucleitin aggregation in Parkinson's disease by disrupting lysosomal membrane permeabilization?

Environmental Exposure _gates_from_environmental_exposure Endolysosomes _gates_to_endolysosomes _gates_from_endolysosomes Lysosomal Membranes _gates_to_lysosomal_membranes _gates_from_lysosomal_membranes Autophagy _gates_to_autophagy

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PathMap Literature Based Discovery Engine

Guaranteed to find unpublished literature based discoveries.

Discovered Hypothesis: Spermidine-mediated autophagic activation may serve as an upstream regulator of lysosomal TMEM175 activity to prevent proteinopathy in C9orf72-ALS/FTD models.

How do electrophilic binding and charge polarity modulate proteinopathy in Alzheimer's Disease, specifically regarding BBB interactions?

Ebola Virus Outbreak Solution Hypothesis: Oral ginger-derived extracellular vesicles may serve as an acid-stable, inexpensive, and supply-chain ready clinical solution to deliver 6-shogaol to macrophages, triggering CASA autophagy to degrade EBOV VP40 and halt viral egress.

Gap Analysis: There is no PubMed data showing wet lab data or analysis of TPD-43 proteinopathy found (or not found) in the Cochlear, Spiral, or Scarpa's Ganglion of Amyotrophic Lateral Sclerosis patient data post mortem.

Parkinson's Disease versus Alzheimer's Disease: Shared and Exclusive Pathways

The use of lysosome-acidifying nanoparticles (AcNPs) could potentially be adapted to treat nanoplastic-induced lysosomal alkalization or membrane rigidification, as these nanoparticles act to restore the degradative capacity lost during environmental contaminant stress.

OGT (O-GlcNAc transferase) modulation via pharmacological agonists can prevent degeneration of cranial nerves following traumatic or surgical stress.

What is Karyoptosis and how does it align with past and present neurodegenerative disease research? Does Karyoptosis provide a new context in which a new class of repurposed therapeutics is formed?

How does autophagy work?

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?

Does existing in vitro data show that Quercetin-induced autophagy can successfully degrade DUX4 or its downstream misfolded proteins?

Does long-term microplastic or bisphenol exposure act as a catalyst for alpha-synucleitin aggregation in Parkinson's disease by disrupting lysosomal membrane permeabilization?