PathMap Literature Based Discovery Engine
Share your Discovery:
Guaranteed to find unpublished literature based discoveries.
Discovery: Vaginal delivery of Hyaluronic Acid-modified Ginger Extracellular Vesicles (HA-GDEVs) co-functionalized with borneol may penetrate fibrotic endometriotic lesions via CD44 targeting, delivering anti-angiogenic payloads to induce lesion regression without systemic hormonal toxicity.


Extracellular Vesicles
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Drug Delivery Systems
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Remission Induction
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Drug-Related Side Effects and Adverse Reactions
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Discovery: Considering PubMed #41177462, intranasal S-GEVs co-functionalized with ApoE peptides may bypass the cribriform plate and target astrocytic LRP1 receptors in order to suppress NF-κB and may resolve some neuroinflammation in Alzheimer's and ALS.


Administration, Intranasal
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Blood-Brain Barrier
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Apolipoproteins E
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Low Density Lipoprotein Receptor-Related Protein-1
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Signal Transduction
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Hypothesis: If Botox were injected into the nerve ending on the third toe on the left foot, the toxin can "climb" retrograde from toe through motor neurons eventually to the brain and temporarily inhibit vesicular docking "from toe to head", potentially allowing a timed pharmacological therapeutic window for toxic EV clearance through the lymph system instead of docking and seeding.


Botulinum Toxins, Type A
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Axonal Transport
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SNARE Proteins
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Lymphatic Vessel Endothelial Hyaluronan Receptor-1
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anti-lamin b1 (phospho t575) antibody - nuclear envelope marker


Ferroptosis


How does the gut microbiome modulate inflammation?


ALS; FUS; STMN2; TDP-43; protein translation; stress granule


Frontotemporal dementia; Splicing; TDP-43; Transcriptomics.


Sarcopenia and Amyotrophic Lateral Sclerosis: Biological Pathways and Analysis


Can fatty liver disease be treated in order to restore gut health?


MASLD pathophysiology
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Gastrointestinal Microbiome
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Farnesoid X-Activated Receptor
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Intestinal Mucosa
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Is TDP-43 proteinopathy associated with toxoplasmosis?


The ALS-T2D comorbidity is driven by a bidirectional, exosome-mediated proteostatic collapse. Peripheral tissues (muscle, pancreas) dictate CNS TDP-43 stability via exosomal miRNAs (miR-126a-5p) and glucose-dependent modifications (O-GlcNAcylation). Conversely, pharmacological activation of ubiquitin-peptidases (e.g., Acarbose targeting USP46) or restitution of glycolytic cofactors (F2,6BP) represent novel, cross-disciplinary therapeutic targets capable of halting systemic proteinopathy.


Diabetes Mellitus, Type 2
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Extracellular Vesicles
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DNA-Binding Proteins
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Amyotrophic Lateral Sclerosis
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