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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 cell biology of beta-amyloid precursor protein and presenilin in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Trends in cell biology 1998-11-01 Risk genes beyond APOE

    It is a truism of modern biomedical science that the development of therapies expected to slow or arrest the progression of a disease requires as detailed an understanding of its molecular and cellular pathogenesis as possible.

  2. Tau pathology in two Dutch families with mutations in the microtubule-binding region of tau

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The American journal of pathology 1998-11-01 Drug development

    Different mutations in the microtubule-associated tau protein gene have recently been identified in several families with hereditary frontotemporal dementia and Parkinsonism (FTDP-17) linked to chromosome 17q21-22.

  3. Activation of tau protein kinase I/glycogen synthase kinase-3beta by amyloid beta peptide (25-35) enhances phosphorylation of tau in hippocampal neurons

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience research 1998-08-01 Drug development

    According to the amyloid hypothesis for the pathogenesis of Alzheimer's disease (AD), amyloid beta peptide (Abeta) directly affects neurons, leading to neurodegeneration and tau phosphorylation, followed by the production of paired helical filaments (PHF) in neurofibrillary tangles (NFT).

  4. The NF-kappaB/Rel family of proteins mediates Abeta-induced neurotoxicity and glial activation

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research. Molecular brain research 1998-06-01 Drug development

    The beta-amyloid peptide (Abeta) is deposited in neuritic plaques which are characteristic features of Alzheimer's disease (AD).

  5. Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson's disease and dementia with Lewy bodies

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The American journal of pathology 1998-04-01 Brain tissue and pathology

    Lewy bodies (LBs) are hallmark lesions of degenerating neurons in the brains of patients with Parkinson's disease (PD) and dementia with Lewy bodies (DLB).

  6. Stabilization of alpha-synuclein secondary structure upon binding to synthetic membranes

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1998-04-01 Brain tissue and pathology

    alpha-Synuclein is a highly conserved presynaptic protein of unknown function.

  7. Mutations in the transmembrane domain of APP altering gamma-secretase specificity

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Biochemistry 1997-12-01 Biomarkers

    Alzheimer's disease (AD) beta-amyloid peptide (Abeta and betaA4) is derived from the amyloid precursor protein (APP) by the subsequent action of the so-far unidentified beta- and gamma-secretases. gamma-secretase, which generates the C-terminus of Abeta, cleaves within the transmembrane domain of APP, preferentially after Abeta-residue 40 (Abeta 40) but also after residue 42 (Abeta 42).

  8. Cellular actions of beta-amyloid precursor protein and its soluble and fibrillogenic derivatives

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Physiological reviews 1997-10-01 Risk genes beyond APOE

    beta-Amyloid precursor protein (beta-APP), the source of the fibrillogenic amyloid beta-peptide (A beta) that accumulates in the brain of victims of Alzheimer's disease, is a multifunctional protein that is widely expressed in the nervous system. beta-Amyloid precursor protein is axonally transported and accumulates in presynaptic terminals and growth cones.

  9. HOP-1, a Caenorhabditis elegans presenilin, appears to be functionally redundant with SEL-12 presenilin and to facilitate LIN-12 and GLP-1 signaling

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-10-01 Drug development

    Mutant presenilins have been found to cause Alzheimer disease.

  10. Lithium reduces tau phosphorylation by inhibition of glycogen synthase kinase-3

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1997-10-01 Drug development

    Lithium is one of the most widely used drugs for treating bipolar (manic-depressive) disorder.

  11. Common core structure of amyloid fibrils by synchrotron X-ray diffraction

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of molecular biology 1997-10-01 Risk factors

    Tissue deposition of normally soluble proteins as insoluble amyloid fibrils is associated with serious diseases including the systemic amyloidoses, maturity onset diabetes, Alzheimer's disease and transmissible spongiform encephalopathy.

  12. Alzheimer presenilins in the nuclear membrane, interphase kinetochores, and centrosomes suggest a role in chromosome segregation

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cell 1997-09-01 Down syndrome and Alzheimer's

    Mutations in two related genes, presenilin 1 and 2, account for most early-onset familial Alzheimer's disease.

  13. Lithium inhibits Alzheimer's disease-like tau protein phosphorylation in neurons

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. FEBS letters 1997-07-01 Drug development

    In Alzheimer's disease, tau protein becomes hyperphosporylated, which can contribute to neuronal degeneration.

  14. Phosphorylation of microtubule-associated protein tau by stress-activated protein kinases

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. FEBS letters 1997-06-01 Drug development

    The paired helical filament, which comprises the major fibrous element of the neurofibrillary lesions of Alzheimer's disease, is composed of hyperphosphorylated microtubule-associated protein tau.

  15. The heat shock-induced hyperphosphorylation of tau is estrogen-independent and prevented by androgens: implications for Alzheimer disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1997-06-01 Drug development

    We have shown that heat shock induces rapid dephosphorylation of tau in both female and male rats followed by hyperphosphorylation only in female rats.

  16. Skeletal and CNS defects in Presenilin-1-deficient mice

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Cell 1997-05-01 Risk genes beyond APOE

    Presenilin-1 (PS1) is the major gene responsible for early-onset familial Alzheimer's disease (FAD).

  17. Amyloid, the presenilins and Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Trends in neurosciences 1997-04-01 Risk genes beyond APOE

    Various mutations in the amyloid protein precursor and presenilin genes can lead to early onset, autosomal Alzheimer's disease.

  18. Human presenilin-1, but not familial Alzheimer's disease (FAD) mutants, facilitate Caenorhabditis elegans Notch signalling independently of proteolytic processing

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Genes and function 1997-04-01 Drug development

    The majority of cases with familial Alzheimer's disease (FAD) are linked to mutations of the presenilin (PS) genes.

  19. Widespread peroxynitrite-mediated damage 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 1997-04-01 Disease mechanisms

    Increasing evidence suggests that oxidative damage to proteins and other macromolecules is a salient feature of the pathology of Alzheimer's disease.

  20. Observation of metastable Abeta amyloid protofibrils by atomic force microscopy

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Chemistry & biology 1997-02-01 Risk genes beyond APOE

    Abeta protofibrils are likely to be intermediates in the in vitro assembly of Abeta amyloid fibrils, but their in vivo role has yet to be determined.

  21. The profile of soluble amyloid beta protein in cultured cell media. Detection and quantification of amyloid beta protein and variants by immunoprecipitation-mass spectrometry

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1996-12-01 Risk genes beyond APOE

    To study the metabolism of amyloid beta protein (Abeta) in Alzheimer's disease, we have developed a new approach for analyzing the profile of soluble Abeta and its variants.

  22. Familial Alzheimer's disease-linked presenilin 1 variants elevate Abeta1-42/1-40 ratio in vitro and in vivo

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 1996-11-01 Risk genes beyond APOE

    Mutations in the presenilin 1 (PS1) and presenilin 2 genes cosegregate with the majority of early-onset familial Alzheimer's disease (FAD) pedigrees.

  23. NACP, a protein implicated in Alzheimer's disease and learning, is natively unfolded

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Biochemistry 1996-10-01 Disease mechanisms

    The "non-A beta component of Alzheimer's disease amyloid plaque" (NAC) is a minor peptide component of the insoluble fibrillar core of the Alzheimer's disease (AD) neuritic plaque.

  24. Endoproteolysis of presenilin 1 and accumulation of processed derivatives in vivo

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 1996-07-01 Risk genes beyond APOE

    The majority of early-onset cases of familial Alzheimer's disease (FAD) are linked to mutations in two related genes, PS1 and PS2, located on chromosome 14 and 1, respectively.

  25. Neurofibrillary tangles of Alzheimer's disease brains contain 14-3-3 proteins

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience letters 1996-05-01 Drug development

    The localisation of 14-3-3 proteins compared to that of tau and ubiquitin-protein conjugates in sections of hippocampus from Alzheimer's disease (AD) brains was examined by immunohistochemistry.

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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