alzhub.org
Get help now — free helplines

You can call any of these for free. You do not need a diagnosis, an appointment, or a crisis to call — questions and plain exhaustion are reasons enough.

  • Alzheimer's Association 24/7 Helpline 800-272-3900 24 hours a day, 365 days a year Free, confidential support and information for people with dementia, caregivers, families and the public. Master's-level clinicians. Also Spanish.
  • 988 Suicide & Crisis Lifeline 988 24/7 Call or text 988, or chat at 988lifeline.org. For anyone in emotional distress or a mental-health crisis, including caregivers.
  • Alzheimer's Foundation of America (AFA) Helpline 866-232-8484 9:00 am - 9:00 pm ET, seven days a week Licensed social workers providing support, info and referrals. Also text message and web chat. Text: 646-586-5283

In a medical emergency, call 911. More numbers, and what each line does, on the help page.

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. Astrocytes expressing hyperphosphorylated tau protein without glial fibrillary tangles in argyrophilic grain disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 1999-09-01 Drug development

    Argyrophilic grain disease (AgD), a frequent type of late onset dementia, is characterized by the occurrence of Gallyas-stained neuropil grains in the hippocampus, entorhinal cortex, amygdala and hypothalamus.

  2. Classification of sporadic Creutzfeldt-Jakob disease based on molecular and phenotypic analysis of 300 subjects

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of neurology 1999-08-01 Brain tissue and pathology

    Phenotypic heterogeneity in sporadic Creutzfeldt-Jakob disease (sCJD) is well documented, but there is not yet a systematic classification of the disease variants.

  3. α-Synuclein Shares Physical and Functional Homology with 14-3-3 Proteins

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Neuroscience 1999-07-15 Brain tissue and pathology

    alpha-Synuclein has been implicated in the pathophysiology of many neurodegenerative diseases, including Parkinson's disease (PD) and Alzheimer's disease.

  4. Impaired synaptic plasticity and learning in aged amyloid precursor protein transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature neuroscience 1999-03-01 Risk genes beyond APOE

    We investigated synaptic communication and plasticity in hippocampal slices from mice overexpressing mutated 695-amino-acid human amyloid precursor protein (APP695SWE), which show behavioral and histopathological abnormalities simulating Alzheimer's disease.

  5. Overexpression of tau protein inhibits kinesin-dependent trafficking of vesicles, mitochondria, and endoplasmic reticulum: implications for Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of cell biology 1998-11-01 Disease mechanisms

    The neuronal microtubule-associated protein tau plays an important role in establishing cell polarity by stabilizing axonal microtubules that serve as tracks for motor-protein-driven transport processes.

  6. Glial cytoplasmic inclusions in white matter oligodendrocytes of multiple system atrophy brains contain insoluble α‐synuclein

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of Neurology 1998-09-01 Brain tissue and pathology

    Recently, alpha-synuclein was shown to be a structural component of the filaments in Lewy bodies (LBs) of Parkinson's disease (PD), dementia with LBs (DLB) as well as the LB variant of Alzheimer's disease, and this suggests that alpha-synuclein could play a mechanistic role in the pathogenesis of these disorders.

  7. Pick's disease: hyperphosphorylated tau protein segregates to the somatoaxonal compartment

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 1996-12-01 Drug development

    Pick bodies and ballooned cells of Pick's disease and the neurofibrillary lesions of Alzheimer's disease are characterized by the presence of hyperphosphorylated microtubule-associated protein tau.

  8. Deficient glutamate tranport is associated with neurodegeneration in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of Neurology 1996-11-01 Disease mechanisms

    The mechanisms of synapse damage in Alzheimer's disease (AD) are not fully understood.

  9. Comparison of neurodegenerative pathology in transgenic mice overexpressing V717F beta-amyloid precursor protein and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PubMed Central 1996-09-15 Disease mechanisms

    Overexpression of mutated human amyloid precursor protein (hAPP717V-->F) under control of platelet-derived growth factor promoter (PDAPP minigene) in transgenic (tg) mice results in neurodegenerative changes similar to Alzheimer's disease (AD).

  10. Amyloid beta protein (Abeta) deposition in chromosome 14-linked Alzheimer's disease: predominance of Abeta42(43)

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of neurology 1996-08-01 Down syndrome and Alzheimer's

    Amyloid beta protein (Abeta) deposition was investigated in the frontal cortex of 8 cases of (genetically confirmed) chromosome 14-linked Alzheimer's disease (AD) using the end-specific monoclonal antibodies BA27 and BC05 to detect the presence of Abeta40 and Abeta42(43), respectively.

  11. Comparison of the neurofibrillary pathology in Alzheimer's disease and familial presenile dementia with tangles

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 1996-07-01 Drug development

    Alzheimer's disease (AD) is characterised neuropathologically by the presence of abundant extracellular beta-amyloid deposits and intracellular neurofibrillary lesions consisting of neurofibrillary tangles, neuropil threads and senile plaque neurites which contain paired helical filaments (PHFs) made of hyperphosphorylated microtubule-associated protein tau.

  12. Trafficking of cell surface beta-amyloid precursor protein: retrograde and transcytotic transport in cultured neurons

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Journal of cell biology 1995-04-01 Drug development

    Amyloid beta-protein (A beta), the principal constituent of senile plaques seen in Alzheimer's disease (AD), is derived by proteolysis from the beta-amyloid precursor protein (beta PP).

  13. Isoform-specific binding of apolipoprotein E to beta-amyloid

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Biological Chemistry 1994-09-01 Genetics

    Apolipoprotein E (apoE), particularly the e4 allele, is genetically linked to the incidence of Alzheimer's disease.

  14. Electron transport chain defects in Alzheimer's disease brain

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurology 1994-06-01 Disease mechanisms

    Previous work suggested a deficiency in the terminal complex of the mitochondrial electron transport chain, cytochrome c oxidase (COX), in platelet mitochondria of Alzheimer's disease (AD) patients.

  15. Expression of alpha B-crystallin in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 1994-01-01 Biomarkers

    alpha B-crystallin is a member of the small heat-shock protein family.

  16. Introduction and expression of the 400 kilobase amyloid precursor protein gene in transgenic mice [corrected]

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature genetics 1993-09-01 Down syndrome and Alzheimer's

    Overexpression of the gene encoding the beta-amyloid precursor protein (APP) may have a key role in the pathogenesis of both Alzheimer's disease (AD) and Down Syndrome (DS).

  17. Complement activation by beta-amyloid in Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Proceedings of the National Academy of Sciences 1992-11-01 Inflammation and the immune system

    Alzheimer disease (AD) is characterized by excessive deposition of the beta-amyloid peptide (beta-AP) in the central nervous system.

  18. Cytochrome oxidase deficiency in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurology 1990-08-01 Disease mechanisms

    We assayed cytochrome oxidase and other electron transport chain activities in platelet mitochondria isolated from patients with Alzheimer's disease (AD).

  19. Pathological proteins Tau 64 and 69 are specifically expressed in the somatodendritic domain of the degenerating cortical neurons during Alzheimer's disease. Demonstration with a panel of antibodies against Tau proteins

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 1990-01-01 Drug development

    Bundles of paired helical filaments (PHF) accumulate in the pyramidal neurons that degenerate during Alzheimer's disease.

  20. Neuritic plaques and cerebrovascular amyloid in Alzheimer disease are antigenically related

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Proceedings of the National Academy of Sciences 1985-12-01 Vascular contributions

    A synthetic peptide (Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr), homologous to the amino terminus of a protein purified from cerebrovascular amyloid (beta protein), induced antibodies in BALB/c mice that were used immunohistochemically to stain not only amyloid-laden cerebral vessels but neuritic plaques as well.

  21. Anti-Aβ Antibody Aducanumab Regulates the Proteome of Senile Plaques and Closely Surrounding Tissue in a Transgenic Mouse Model of Alzheimer’s Disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of Alzheimer's Disease 2021-01-05 Treatments

    In the aducanumab-treated mice, we identified 17 significantly regulated proteins that were associated with 1) mitochondria and metabolism (ACAT2, ATP5J, ETFA, EXOG, HK1, NDUFA4, NDUFS7, PLCB1, PPP2R4), 2) cytoskeleton and axons (ADD1, CAPZB, DPYSL3, MAG), 3) stress response (HIST1H1C/HIST1H1D, HSPA12A), and 4) AβPP trafficking/processing (CD81, GDI2).

  22. REDD1 Is Involved in Amyloid β-Induced Synaptic Dysfunction and Memory Impairment

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. International journal of molecular sciences 2020-12-13 Disease mechanisms

    Alzheimer's disease (AD) is a neurodegenerative disease characterized by neurological dysfunction, including memory impairment, attributed to the accumulation of amyloid β (Aβ) in the brain.

  23. Targeting Tau to Treat Clinical Features of Huntington's Disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Frontiers in neurology 2020-11-19 Drug development

    Huntington's disease (HD) is an autosomal dominant neurodegenerative disorder characterized by severe motor, cognitive and psychiatric impairments.

  24. The Role of ADF/Cofilin in Synaptic Physiology and Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Frontiers in cell and developmental biology 2020-11-12 Disease mechanisms

    Actin-depolymerization factor (ADF)/cofilin, a family of actin-binding proteins, are critical for the regulation of actin reorganization in response to various signals.

  25. Autophagy and heat-shock response impair stress granule assembly during cellular senescence

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Mechanisms of ageing and development 2020-10-10 Disease mechanisms

    Stress granules (SGs) are membraneless organelles formed in response to insult.

Other topics