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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. Ultrastructural localization of beta-amyloid, tau, and ubiquitin epitopes in extracellular neurofibrillary tangles

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1991-03-01 Drug development

    Neurofibrillary tangles (NFTs), a hallmark of Alzheimer disease, are commonly located in perikarya of neurons.

  2. Advances in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The FASEB Journal 1991-03-01 Disease mechanisms

    The problem of the etiology of Alzheimer's disease has not been solved.

  3. Antibodies to non-beta regions of the beta-amyloid precursor protein detect a subset of senile plaques

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The American journal of pathology 1991-02-01 Drug development

    A central unresolved issue in Alzheimer's disease is the origin of the extracellular amyloid beta protein (A beta P) found in senile plaques and its relationship to the dystrophic neurites that intimately surround it.

  4. Tau in Alzheimer neurofibrillary tangles. N- and C-terminal regions are differentially associated with paired helical filaments and the location of a putative abnormal phosphorylation site

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Biochemical journal 1991-01-01 Drug development

    To investigate the extent to which whole tau proteins, structurally abnormal tau and fragments of tau are incorporated into neurofibrillary tangles in Alzheimer's disease, an immunocytochemical mapping study using a panel of antibodies to several synthetic human tau peptides has been performed.

  5. A4 protein in Alzheimer's disease: primary and secondary cellular events in extracellular amyloid deposition

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neuropathology and experimental neurology 1989-11-01 Biomarkers

    This study was designed to investigate the role of serum proteins, microglia, glial fibrillary acidic protein (GFAP) positive cells and dystrophic neurites in the genesis of cerebral amyloid.

  6. Identification, biogenesis, and localization of precursors of Alzheimer's disease A4 amyloid protein

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cell 1989-04-01 Tau biomarkers

    To study the putative precursor proteins (PreA4(695), PreA4(751), and PreA4(770] of Alzheimer's disease A4 amyloid protein, polyclonal and monoclonal antibodies were raised against a recombinant bacterial PreA4(695) fusion protein.

  7. Microtubule-associated polypeptides tau are altered in Alzheimer paired helical filaments

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research 1988-08-01 Drug development

    Antisera were raised in rabbits to purified bovine tau and to isolated Alzheimer paired helical filaments (PHF) washed with sodium dodecyl sulfate (SDS).

  8. Immunochemical and biochemical characterization of tau proteins in normal and Alzheimer's disease brains with Alz 50 and Tau-1

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1988-06-01 Drug development

    Microtubule-associated protein tau was characterized in 5 Alzheimer and 5 control brains using two monoclonal antibodies, Alz 50 and Tau-1.

  9. Immunochemical identification of the serine protease inhibitor alpha 1-antichymotrypsin in the brain amyloid deposits of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cell 1988-02-01 Treatments

    Two approaches--molecular cloning and immunochemical analysis--have identified one of the components of Alzheimer's disease amyloid deposits as the serine protease inhibitor alpha 1-antichymotrypsin.

  10. Purification and characterization of a peptide from amyloid-rich pancreases of type 2 diabetic patients

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1987-12-01 Risk factors

    Deposition of amyloid in pancreatic islets is a common feature in human type 2 diabetic subjects but because of its insolubility and low tissue concentrations, the structure of its monomer has not been determined.

  11. Alzheimer's neurofibrillary tangles contain unique epitopes and epitopes in common with the heat-stable microtubule associated proteins tau and MAP2

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The American journal of pathology 1987-01-01 Drug development

    Ten monoclonal antibodies raised against Alzheimer's neurofibrillary tangles (ANTs) were characterized for reactivity with heat-stable microtubule fractions from bovine and human brain.

  12. The neurobiologic consequences of Down syndrome

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research bulletin 1986-06-01 Down syndrome and Alzheimer's

    Trisomy of the whole or distal part of human chromosome 21 (HSA 21) (Ts21) results in Down Syndrome (DS), which is characterized in part by mental retardation and associated neurological abnormalities.

  13. Cholinergic innervation of cortex by the basal forebrain: Cytochemistry and cortical connections of the septal area, diagonal band nuclei, nucleus basalis (Substantia innominata), and hypothalamus in the rhesus monkey

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of Comparative Neurology 1983-02-20 Risk factors

    In Alzheimer's disease, the relatively selective depression of neocortical cholinergic innervation may be closely associated with the neuronal loss in Ch4, which has also been described inthis condition.

  14. APH-1A and CDK5 Expression Correlates with Tau Hyperphosphorylation and Its Attenuation by Brahmi and Donep-M in STZ induced Alzheimer’s Disease Model

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-31 Genetics

    Alzheimer’s disease (AD) is a progressively characterized neurodegenerative condition marked by molecular instability, neuronal dysfunction and abnormal tau buildup.

  15. The Alzheimer's disease-associated rs28834970 variant in PTK2B impairs electrical activity and regulates Tau phosphorylation and APP processing in human neuronal cultures

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30 Genetics

    The rs28834970 regulatory variant was identified as the most functionally relevant in our model, with the C risk allele promoting transcription factor C/EBPβ binding within a cis-regulatory element.

  16. Disrupting SORL1-retromer endosomal recycling in mice drives the age-dependent neurodegenerative signature of Alzheimer's disease

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30 Genetics

    MRI studies have mapped the atrophic signature that distinguishes Alzheimer's disease (AD), isolating regions differentially vulnerable to its age-dependent neurodegenerative process.

  17. Opposing Regulation of Tau Condensation by Phosphorylation Levels and Molecular Chaperone Interactions

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30 Treatments

    Aggregation of the microtubule-stabilizing protein Tau into insoluble deposits is characteristic for several neurodegenerative diseases, including Alzheimer's disease.

  18. TMEM106B C-Terminal fragment aggregation exacerbates α-synuclein and TDP-43 proteinopathy phenotypes

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-30 Brain tissue and pathology

    Genetic variation in the human gene encoding the lysosomal transmembrane protein 106B (TMEM106B) drives risk of neurodegenerative dementia.

  19. SHED-Derived Exosomes Attenuate Alzheimer's Disease Pathology in iPSC-Derived Cerebral Organoid Model

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-29 Biomarkers

    SHED exosome treatment demonstrated genotype-specific efficacy, selectively reducing p181-tau levels and restoring the p181-tau/Aβ42 ratio in FAD lines while elevating the protective Aβ42/Aβ40 ratio across both FAD and SAD backgrounds.

  20. Effect of Metformin on tau pathology and proteostasis in cellular and a Drosophila model of Tauopathy

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-29 Drug development

    Alzheimer’s disease is increasingly linked to metabolic dysfunction, with insulin resistance emerging as a key contributor to tau pathology.

  21. Aβ42 oligomers disrupt calcium homeostasis via Piezo1 and induce neurotoxicity in differentiated SH-SY5Y cells

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-29 Disease mechanisms

    Alzheimer's disease (AD) exhibits an intricate and multifactorial pathogenesis.

  22. Neuronal Hyperactivity Induces Tau Phosphorylation Selectively in Excitatory Pyramidal Neurons Which Contributes to GluA2 Regulation

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-28 Disease mechanisms

    While tau plays a role in regulating neuronal network excitability, a process thought to be dysregulated in Alzheimer’s disease (AD), the molecular mechanisms linking tau and hyperexcitability remain unclear.

  23. Second-generation tau PET tracer in situ binding assessed with fluorescence imaging

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-10-27 Brain scans and imaging

    Brain positron emission tomography (PET) imaging is a valuable tool which allows visualization of the pathological structures inside the living patients’ brains.

  24. Repeated VU0155069 Treatment Is Associated with Region- and Pathological Stage-Specific Dendritic Spine Remodeling in Female 3xTg-AD Mice

    ⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27 Brain tissue and pathology

    VU0155069 engages circuit- and pathological stage-specific forms of dendritic spine remodeling across distributed recognition- and associative-memory networks.

  25. The Filamin A Proteomic Switch: Solubility States and Cytoskeletal Dynamics Explain the Inverse Epidemiological Relationship Between Cancer and Alzheimer’s Disease

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

    This structural configuration shields the scaffold from calpain-mediated cleavage, reconfiguring FLNA into an active motility engine driving invasive lamellipodia but stalls proteolytic processing and forces an absolute loss of the nuclear FLNA-90 tumor-suppressor brake, unleashing uninhibited c-Myc oncogenic transcription.

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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