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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. The pharmacology of sigma-1 receptors

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Pharmacology & therapeutics 2009-07-18 Brain scans and imaging

    Originally considered an enigmatic protein, the sigma-1 receptor has recently been identified as a unique ligand-regulated molecular chaperone in the endoplasmic reticulum of cells.

  2. (-)-epigallocatechin-3-gallate (EGCG) maintains kappa-casein in its pre-fibrillar state without redirecting its aggregation pathway

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of molecular biology 2009-07-17 Treatments

    The polyphenol (-)-epigallocatechin-3-gallate (EGCG) has recently attracted much research interest in the field of protein-misfolding diseases because of its potent anti-amyloid activity against amyloid-beta, alpha-synuclein and huntingtin, the amyloid-fibril-forming proteins involved in Alzheimer's, Parkinson's and Huntington's diseases, respectively.

  3. Amyloid-β protein oligomerization and the importance of tetramers and dodecamers in the aetiology of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Nature chemistry 2009-07-01 Risk factors

    In recent years, small protein oligomers have been implicated in the aetiology of a number of important amyloid diseases, such as type 2 diabetes, Parkinson's disease and Alzheimer's disease.

  4. Impaired balance of mitochondrial fission and fusion in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2009-07-01 Disease mechanisms

    Mitochondrial dysfunction is a prominent feature of Alzheimer's disease (AD) neurons.

  5. Decreased brain-derived neurotrophic factor depends on amyloid aggregation state in transgenic mouse models of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2009-07-01 Down syndrome and Alzheimer's

    Downregulation of brain-derived neurotrophic factor (BDNF) in the cortex occurs early in the progression of Alzheimer's disease (AD).

  6. Soluble oligomers of amyloid Beta protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2009-06-01 Risk factors

    In Alzheimer's disease (AD), the impairment of declarative memory coincides with the accumulation of extracellular amyloid-beta protein (Abeta) and intraneuronal tau aggregates.

  7. Gold nanoparticles in nanomedicine: preparations, imaging, diagnostics, therapies and toxicity

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Chemical Society reviews 2009-04-21 Risk factors

    This critical review provides an overall survey of the basic concepts and up-to-date literature results concerning the very promising use of gold nanoparticles (AuNPs) for medicinal applications.

  8. Alpha-Synuclein contributes to GSK-3beta-catalyzed Tau phosphorylation in Parkinson's disease models

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. FASEB journal : official publication of the Federation of American Societies for Experimental Biology 2009-04-15 Drug development

    We have shown in the parkinsonism-inducing neurotoxin MPP(+)/MPTP model that alpha-Synuclein (alpha-Syn), a presynaptic protein causal in Parkinson's disease (PD), contributes to hyperphosphorylation of Tau (p-Tau), a protein normally linked to tauopathies, such as Alzheimer's disease (AD).

  9. Comparison of Abeta levels in the brain of familial and sporadic Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurochemistry international 2009-03-20 Biomarkers

    Mutations in presenilin (PS) and amyloid precursor protein (APP) genes are a predominant cause for early-onset familial Alzheimer disease (AD).

  10. Oligomeric amyloid beta associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-02-19 Disease mechanisms

    Synapse loss correlates with a cognitive decline in Alzheimer's disease (AD), but whether this is caused by fibrillar deposits known as senile plaques or soluble oligomeric forms of amyloid beta (Abeta) is controversial.

  11. Protection of synapses against Alzheimer's-linked toxins: insulin signaling prevents the pathogenic binding of Abeta oligomers

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-02-02 Disease mechanisms

    Synapse deterioration underlying severe memory loss in early Alzheimer's disease (AD) is thought to be caused by soluble amyloid beta (Abeta) oligomers.

  12. Mitochondrial dysfunction and glaucoma

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of glaucoma 2009-02-01 Brain scans and imaging

    Glaucoma is increasingly recognized as a neurodegenerative disorder, characterized by the accelerated loss of retinal ganglion cells (RGCs) and their axons.

  13. Development of tau aggregation inhibitors for Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Angewandte Chemie (International ed. in English) 2009-01-01 Drug development

    A variety of human diseases are suspected to be directly linked to protein misfolding.

  14. Biological and chemical approaches to diseases of proteostasis deficiency

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Annual review of biochemistry 2009-01-01 Disease mechanisms

    Many diseases appear to be caused by the misregulation of protein maintenance.

  15. Impairing the mitochondrial fission and fusion balance: a new mechanism of neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Annals of the New York Academy of Sciences 2008-12-01 Risk factors

    Mitochondrial dysfunction is a common characteristic of all neurodegenerative diseases.

  16. Mitochondria in neuroplasticity and neurological disorders

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2008-12-01 Disease mechanisms

    Mitochondrial electron transport generates the ATP that is essential for the excitability and survival of neurons, and the protein phosphorylation reactions that mediate synaptic signaling and related long-term changes in neuronal structure and function.

  17. Picomolar amyloid-beta positively modulates synaptic plasticity and memory in hippocampus

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2008-12-01 Disease mechanisms

    Amyloid-beta (Abeta) peptides are produced in high amounts during Alzheimer's disease, causing synaptic and memory dysfunction.

  18. Molecular structural basis for polymorphism in Alzheimer's beta-amyloid fibrils

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2008-11-17 Risk factors

    We describe a full structural model for amyloid fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease (Abeta(1-40)), based on numerous constraints from solid state NMR and electron microscopy.

  19. Proteomics of the lysosome

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Biochimica et biophysica acta 2008-10-15 Genetics

    Defects in lysosomal function have been associated with numerous monogenic human diseases typically classified as lysosomal storage diseases.

  20. Parkinsonism and impaired axonal transport in a mouse model of frontotemporal dementia

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2008-10-02 Digital health tools

    Frontotemporal dementia (FTD) is characterized by cognitive and behavioral changes and, in a significant subset of patients, Parkinsonism.

  21. Beta-amyloid deposition and functional impairment in the retina of the APPswe/PS1DeltaE9 transgenic mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Investigative ophthalmology & visual science 2008-09-12 Biomarkers

    The present findings suggest that Abeta deposition disrupts retinal structure and may contribute to the visual deficits seen in aged APPswe/PS1DeltaE9 tg mice.

  22. The amyloid beta-peptide is imported into mitochondria via the TOM import machinery and localized to mitochondrial cristae

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2008-08-29 Disease mechanisms

    The amyloid beta-peptide (Abeta) has been suggested to exert its toxicity intracellularly.

  23. Wnt signaling in neuroprotection and stem cell differentiation

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Progress in neurobiology 2008-08-19 Drug development

    In the past several years, we postulated that the loss of Wnt signaling was implicated in the pathology of Alzheimer's disease (AD).

  24. New insights into brain BDNF function in normal aging and Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research reviews 2008-08-03 Disease mechanisms

    The decline observed during aging involves multiple factors that influence several systems.

  25. Neuronal calcium mishandling and the pathogenesis of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Trends in neurosciences 2008-07-31 Risk genes beyond APOE

    Perturbed neuronal Ca(2+) homeostasis is implicated in age-related cognitive impairment and Alzheimer's disease (AD).

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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