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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.

Download bibliography of all 1,352 studies, highest score first: BibTeX (.bib) · RIS (.ris)

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

  1. Positively Charged Polyprodrug Amphiphiles with Enhanced Drug Loading and Reactive Oxygen Species-Responsive Release Ability for Traceable Synergistic Therapy

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of the American Chemical Society 2018-03-07 Drug development

    Due to the vast differences in chemical properties among small molecule drugs, nucleotide drugs, and superparamagnetic iron oxide nanocubes (SPIONs), such as charge and hydrophobicity, entrapment of these within a single carrier for traceable synergistic therapy has been proven difficult.

  2. Amyloid fibril polymorphism: a challenge for molecular imaging and therapy

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of internal medicine 2018-02-19 End-of-life care

    The accumulation of misfolded proteins (MPs), both unique and common, for different diseases is central for many chronic degenerative diseases.

  3. NAD + supplementation normalizes key Alzheimer's features and DNA damage responses in a new AD mouse model with introduced DNA repair deficiency

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2018-02-05 Disease mechanisms

    Emerging findings suggest that compromised cellular bioenergetics and DNA repair contribute to the pathogenesis of Alzheimer's disease (AD), but their role in disease-defining pathology is unclear.

  4. Tau-Targeted Multifunctional Nanocomposite for Combinational Therapy of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. ACS nano 2018-02-01 Drug development

    Alzheimer's disease (AD) remains an incurable disease and lacks efficient diagnostic methods.

  5. Wnt signaling loss accelerates the appearance of neuropathological hallmarks of Alzheimer's disease in J20-APP transgenic and wild-type mice

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of neurochemistry 2018-01-26 Biomarkers

    Alzheimer's disease (AD) is a neurodegenerative pathology characterized by aggregates of amyloid-β (Aβ) and phosphorylated tau protein, synaptic dysfunction, and spatial memory impairment.

  6. iPSC-Based Compound Screening and In Vitro Trials Identify a Synergistic Anti-amyloid β Combination for Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Cell reports 2017-11-01 Treatments

    In the process of drug development, in vitro studies do not always adequately predict human-specific drug responsiveness in clinical trials.

  7. Dysfunction of autophagy and endosomal-lysosomal pathways: Roles in pathogenesis of Down syndrome and Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Free radical biology & medicine 2017-10-06 Down syndrome and Alzheimer's

    Individuals with Down syndrome (DS) have an increased risk of early-onset Alzheimer's Disease (AD), largely owing to a triplication of the APP gene, located on chromosome 21.

  8. Tauopathy and cognitive impairment in experimental diabetes mellitus

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Diabetes mellitus 2017-08-10 Risk factors

    Currently, diabetes mellitus (DM) is the most common metabolic disorder, which is manifested by hyperglycemia and leads to vascular and cognitive impairment.

  9. Amyloid beta: structure, biology and structure-based therapeutic development

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Acta pharmacologica Sinica 2017-07-17 Risk genes beyond APOE

    Amyloid beta peptide (Aβ) is produced through the proteolytic processing of a transmembrane protein, amyloid precursor protein (APP), by β- and γ-secretases.

  10. Cortical influences drive amyotrophic lateral sclerosis

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of neurology, neurosurgery, and psychiatry 2017-07-14 Digital health tools

    The early motor manifestations of sporadic amyotrophic lateral sclerosis (ALS), while rarely documented, reflect failure of adaptive complex motor skills.

  11. Aβ seeding potency peaks in the early stages of cerebral β-amyloidosis

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. EMBO reports 2017-07-12 Biomarkers

    Little is known about the extent to which pathogenic factors drive the development of Alzheimer's disease (AD) at different stages of the long preclinical and clinical phases.

  12. Genetics of β-Amyloid Precursor Protein in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Cold Spring Harbor perspectives in medicine 2017-06-01 Down syndrome and Alzheimer's

    Alzheimer's disease (AD) is characterized neuropathologically by neuronal cell loss, extracellular neuritic plaques composed of β-amyloid (Aβ), and intracellular neurofibrillary tangles composed of hyperphosphorylated tau protein.

  13. Protein Misfolding, Amyloid Formation, and Human Disease: A Summary of Progress Over the Last Decade

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Annual review of biochemistry 2017-05-12 Risk factors

    Peptides and proteins have been found to possess an inherent tendency to convert from their native functional states into intractable amyloid aggregates.

  14. Liraglutide Improves Water Maze Learning and Memory Performance While Reduces Hyperphosphorylation of Tau and Neurofilaments in APP/PS1/Tau Triple Transgenic Mice

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neurochemical research 2017-04-06 Drug development

    The purpose of this study was to explore how liraglutide affects AD-like pathology and cognitive function in APP/PS1/Tau triple transgenic (3 × Tg) Alzheimer disease (AD) model mice.

  15. Individuals with progranulin haploinsufficiency exhibit features of neuronal ceroid lipofuscinosis

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Science translational medicine 2017-04-01 Brain scans and imaging

    Heterozygous mutations in the GRN gene lead to progranulin (PGRN) haploinsufficiency and cause frontotemporal dementia (FTD), a neurodegenerative syndrome of older adults.

  16. Mitophagy and Alzheimer's Disease: Cellular and Molecular Mechanisms

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Trends in neurosciences 2017-02-09 Disease mechanisms

    Neurons affected in Alzheimer's disease (AD) experience mitochondrial dysfunction and a bioenergetic deficit that occurs early and promotes the disease-defining amyloid beta peptide (Aβ) and Tau pathologies.

  17. Cytosolic Fc receptor TRIM21 inhibits seeded tau aggregation

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2017-01-03 Drug development

    Alzheimer's disease (AD) and other neurodegenerative disorders are associated with the cytoplasmic aggregation of microtubule-associated protein tau.

  18. Role of Glutamate and NMDA Receptors in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of Alzheimer's disease : JAD 2017-01-01 Treatments

    Excitatory glutamatergic neurotransmission via N-methyl-d-aspartate receptor (NMDAR) is critical for synaptic plasticity and survival of neurons.

  19. Amyloid-Beta and Phosphorylated Tau Accumulations Cause Abnormalities at Synapses of Alzheimer's disease Neurons

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Journal of Alzheimer's disease : JAD 2017-01-01 Disease mechanisms

    Amyloid-beta (Aβ) and hyperphosphorylated tau are hallmark lesions of Alzheimer's disease (AD).

  20. Proteostasis regulation by the ubiquitin system

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Essays in biochemistry 2016-10-15 Disease mechanisms

    Cells have developed an evolutionary obligation to survey and maintain proteome fidelity and avoid the possible toxic consequences of protein misfolding and aggregation.

  21. Interrelationship between Changes in the Amyloid β 42/40 Ratio and Presenilin 1 Conformation

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Molecular medicine (Cambridge, Mass.) 2016-07-05 Biomarkers

    The ratio of the longer (i.e., Aβ42/Aβ43) to shorter (i.e. Aβ40) species is a critical factor determining amyloid fibril formation, neurotoxicity and progression of the amyloid pathology in Alzheimer's disease.

  22. Ubiquitin-dependent and independent roles of SUMO in proteostasis

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. American journal of physiology. Cell physiology 2016-06-22 Disease mechanisms

    Cellular proteomes are continuously undergoing alterations as a result of new production of proteins, protein folding, and degradation of proteins.

  23. Impaired protein degradation in FTLD and related disorders

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Ageing research reviews 2016-05-07 Disease mechanisms

    Impaired protein degradation has been discussed as a cause or consequence of various neurodegenerative diseases, such as Alzheimer's, Parkinson's and Huntington's disease.

  24. Apolipoprotein E lipoprotein particles inhibit amyloid-β uptake through cell surface heparan sulphate proteoglycan

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Molecular neurodegeneration 2016-05-05 Genetics

    In this study, we show that apoE lipoprotein particles from conditioned media of immortalized astrocytes isolated from human APOE-targeted replacement (TR) mice significantly suppress cellular Aβ42 and Aβ40 uptake through cell surface HSPG.

  25. Familial Alzheimer's Disease Mutations in Presenilin Generate Amyloidogenic Aβ Peptide Seeds

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neuron 2016-04-20 Risk genes beyond APOE

    Recently it was proposed that the familial Alzheimer's disease (FAD) causing presenilin (PSEN) mutations PSEN1-L435F and PSEN1-C410Y do not support the generation of Aβ-peptides from the amyloid precursor protein (APP).

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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