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Home › Research › Topic

Disease mechanisms in lab and animal studies

1,352 studies in this group. A computer grouped them by what their titles and summaries are about, not by a hand-made list. The name describes most of the group, not every study in it.

Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.

Highest usefulness score first. Studies without a score come last.

  1. Precision Nanocrystal Theranostics for Neurodegenerative Proteopathies: Strategies to Cross the Blood-Brain Barrier and Target Protein Aggregation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2026-10-26 Vascular contributions

    This review examines nanocrystal-based theranostic platforms as a promising method to overcome the blood-brain barrier (BBB) in neurodegenerative diseases like Alzheimer’s and Parkinson’s. These neurological diseases involve gradual protein misfolding and aggregation, causing neuronal damage and loss.

  2. Anti-GABA B receptor autoimmunity causes cognitive decline by presynaptic pathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-25 Disease mechanisms

    The GABA B receptor is a central regulator of neuronal transmission and excitability by pre- and postsynaptic mechanisms.

  3. Temporal Proteomics Links the APP London Mutation to Early Cholesterol Remodeling Cell Programs in Human Neurons

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-24 Risk genes beyond APOE

    Familial Alzheimer’s disease (AD) mutations in amyloid precursor protein (APP) alter amyloid-β (Aβ) secretion profiles, but their effects on neuronal protein and lipid homeostasis remain incompletely understood.

  4. TMEM55B downregulation promotes neurodegeneration in Alzheimer’s disease models

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-24 Brain scans and imaging

    Lysosomal distribution is critical for numerous biological functions within the cell, including protein degradation in autophagosomes, cholesterol homeostasis, and cell invasion.

  5. Astrocytic ablation of truncated TrkB receptors reduces amyloid plaques and prevents synaptic loss in 5xFAD mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-24 Inflammation and the immune system

    Together, these findings identify astrocytic TrkB.T as an important regulator of amyloid pathology and synaptic integrity in an AD mouse model.

  6. Early Insulin Signaling Abnormalities and Oxidative Stress Responses in PS19 Tau Transgenic Mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-22 Inflammation and the immune system

    Pathological tau accumulation is a hallmark of Alzheimer’s disease (AD), yet its relationship with impaired insulin signaling remains unclear.

  7. Discovery of a brain-penetrant CHI3L1 inhibitor as an oral modulator of neuroinflammation in Alzheimers disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-21 Tau biomarkers

    Chitinase-3-like protein 1 (CHI3L1) is elevated in Alzheimers disease (AD), but its role in glial dysfunction and therapeutic tractability remain unclear.

  8. SpineTool 2.0: A Deep Learning Platform with an Interactive User Interface for Dendritic Spine Segmentation and Morphological Analysis

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-21 Disease mechanisms

    Quantitative analysis of dendritic spine morphology is central to understanding synaptic function and its disruption in neurological disease, yet reliable measurement depends on accurate segmentation of spines from fluorescence microscopy images — a task still limited by faint or discontinuous spine necks and by tools that require extensive manual correction.

  9. Natural Sesquiterpenoids from Laggera pterodonta as bioactive Acetylcholinesterase Inhibitors: Insights from DFT, Molecular Docking, and ADMET Profiling

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-20 Treatments

    Alzheimer's disease continues to be one of the major critical neurodegenerative ailments of the modern era, with acetylcholinesterase (AChE) inhibition standing as a foundational therapeutic strategy.

  10. Stimulating microglial neuroinflammation with amyloid-beta oligomers compatible with solid-state NMR structural characterization

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-20 Inflammation and the immune system

    Soluble amyloid-β (Aβ) oligomers are considered the primary neurotoxic species in Alzheimer’s disease, yet the relationship between oligomer structure and biological activity remains poorly understood.

  11. BNIP3L/NIX-mediated mitophagy limits Alzheimer’s disease pathology and preserves neuronal function

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-20 Disease mechanisms

    Defective mitophagy is emerging as a key contributor to Alzheimer’s disease (AD), but the neuronal pathways governing mitochondrial clearance and their contribution to disease progression remain poorly understood.

  12. LATS2 modulates synaptic organization and function by regulating actin dynamics

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-19 Disease mechanisms

    Recent work has highlighted the importance of core Hippo pathway kinases in cycling cells.

  13. The Alzheimer’s disease risk gene ABCA7 regulates microglial lysosomal and lipid homeostasis and promotes phagocytosis to maintain neuronal health

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-19 Disease mechanisms

    ABCA7-KO iMGs were deficient for proteins involved in lysosome function, measured by down-regulated lysosomal proteomic signatures, as well as reduced DQ-BSA activity and reduced LAMP1+ area.

  14. DNA-Encoded Library-Guided Discovery of a First-in-Class Molecular Glue of the NOS1AP-SCRIB Complex in Alzheimer’s Disease Patient-Derived Neurons

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-18 Biomarkers

    NOS1AP is an adaptor for neuronal nitric oxide synthase that engages several partner proteins and is implicated in Alzheimer’s disease.

  15. Mapping post-translational modifications across amyloid-β deposits in Alzheimer’s disease: A neuropathologic survey with in vitro functional analysis of nitration

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-18 Treatments

    Distinct PTMs delineate the compartment-specific architectural signatures of Aβ deposits.

  16. Progressive neurodegeneration of the locus coeruleus drives rapid eye movement sleep fragmentation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-16 Brain scans and imaging

    Sleep disturbances are common early features of neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD).

  17. Reduced phosphatases and hyperphosphorylated glutamatergic receptors persist from early to late stages of prion disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-16 Disease mechanisms

    Synapse loss occurs early in prion disease, yet the intracellular signaling driving this dysregulation remains poorly understood.

  18. Integrative Multiomics Analysis Reveals a Coordinated Molecular Signature of Neuroresilience in human MAPT-knockout hiPSC-derived Neurons with relevance for Alzheimer’s and Neurodegenerative Disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-14 Disease mechanisms

    These findings demonstrate that Tau deletion induces an active, multilevel gain-of-resilience rather than passive resistance.

  19. Intrastriatal injection of amplified Lewy body dementia (LBD) fibrils in mice results in accumulation of fibrils with LBD structure and neurodegeneration

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-13 Brain tissue and pathology

    The defining neuropathologic feature of Lewy body dementia (LBD) and Parkinson’s disease (PD) is alpha-synuclein (Asyn) fibril accumulation in Lewy bodies (LBs) and Lewy neurites (LNs).

  20. ALS-associated mutations reveal a conserved C-terminal self-assembly module in the TDP-43 low-complexity domain

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-12 Brain tissue and pathology

    TAR DNA-binding protein 43 (TDP-43) is an RNA-binding protein whose low-complexity domain (LCD) mediates self-assembly, liquid-liquid phase separation, and pathological aggregation associated with amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD).

  21. An astrocyte-neuron HSPB1 axis preserves lysosomal integrity and protects from tau pathology

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-12 Disease mechanisms

    Alzheimer’s disease (AD) is characterized by a decline in neuronal proteostasis that favours the accumulation of misfolded proteins.

  22. PDE4D inhibition activates cAMP-PKA signaling to preserve mitochondrial homeostasis and prevent neuronal necroptosis in Alzheimer's disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-12 Disease mechanisms

    Alzheimer’s disease involves progressive necroptosis of neurons, and the associated cognitive deficits can be mitigated by inhibiting cAMP-degrading phosphodiesterase 4D (PDE4D).

  23. Carbonic anhydrase inhibition rescues heart function in the Tg2576 Alzheimer’s mouse model by ameliorating cardiac amyloid-β pathology and neurotrophic-signaling impairment

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-09 Vascular contributions

    FDA-approved carbonic anhydrase inhibitors (CAIs) have shown robust efficacy in reducing amyloid-β (Aβ) pathology, neurodegeneration, and cerebrovascular dysfunction in Alzheimer’s disease (AD) and cerebral amyloid angiopathy (CAA) models, highlighting carbonic anhydrase (CAs) as a promising, previously untapped therapeutic target for AD and vascular contribution to dementia.

  24. A First-in-Class, Brain-Penetrant Small Molecule Inhibitor of the NOS1AP-Tau Interaction Rescues Tau Pathology In Vivo and Improves Cognition

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-07 Biomarkers

    NOS1AP is a genetically validated driver of tau pathology in Alzheimer’s disease (AD), yet the NOS1AP-tau interaction itself has remained pharmacologically untargeted.

  25. Brain region- and solubility-dependent proteomic signatures of neurofibrillary tangle pathology in Alzheimer’s disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-07 Brain tissue and pathology

    Neurofibrillary tangles (NFTs) containing hyperphosphorylated tau proteins are a hallmark neuropathology of Alzheimer’s disease.

From across this topic

10 of the 1,352 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.

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