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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. Axonopathy and transport deficits early in the pathogenesis of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2005-02-01 Risk genes beyond APOE

    We identified axonal defects in mouse models of Alzheimer's disease that preceded known disease-related pathology by more than a year; we observed similar axonal defects in the early stages of Alzheimer's disease in humans.

  2. Abeta localization in abnormal endosomes: association with earliest Abeta elevations in AD and Down syndrome

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Neurobiology of aging 2004-11-01 Down syndrome and Alzheimer's

    Early endosomes are a major site of amyloid precursor protein (APP) processing and a convergence point for molecules of pathologic relevance to Alzheimer's disease (AD).

  3. ABAD directly links Abeta to mitochondrial toxicity in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 2004-04-01 Prevention and risk

    Mitochondrial dysfunction is a hallmark of beta-amyloid (Abeta)-induced neuronal toxicity in Alzheimer's disease (AD).

  4. GSK-3alpha regulates production of Alzheimer's disease amyloid-beta peptides

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2003-05-01 Risk genes beyond APOE

    Alzheimer's disease is associated with increased production and aggregation of amyloid-beta (Abeta) peptides.

  5. The role of presenilin cofactors in the gamma-secretase complex

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2003-03-16 Risk genes beyond APOE

    Mutations in presenilin genes account for the majority of the cases of the familial form of Alzheimer's disease (FAD).

  6. Neurodegenerative disease: amyloid pores from pathogenic mutations

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2002-07-01 Brain tissue and pathology

    Alzheimer's and Parkinson's diseases are associated with the formation in the brain of amyloid fibrils from beta-amyloid and alpha-synuclein proteins, respectively.

  7. A beta peptide immunization reduces behavioural impairment and plaques in a model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2000-12-01 Risk genes beyond APOE

    Much evidence indicates that abnormal processing and extracellular deposition of amyloid-beta peptide (A beta), a proteolytic derivative of the beta-amyloid precursor protein (betaAPP), is central to the pathogenesis of Alzheimer's disease (reviewed in ref. 1).

  8. Photoactivated gamma-secretase inhibitors directed to the active site covalently label presenilin 1

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 2000-06-01 Risk genes beyond APOE

    Cleavage of amyloid precursor protein (APP) by the beta- and gamma-secretases generates the amino and carboxy termini, respectively, of the A beta amyloidogenic peptides A beta40 and A beta42--the major constituents of the amyloid plaques in the brain parenchyma of Alzheimer's disease patients.

  9. A presenilin-1-dependent gamma-secretase-like protease mediates release of Notch intracellular domain

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1999-04-01 Risk genes beyond APOE

    Signalling through the receptor protein Notch, which is involved in crucial cell-fate decisions during development, requires ligand-induced cleavage of Notch.

  10. Presenilin is required for activity and nuclear access of Notch in Drosophila

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1999-04-01 Risk genes beyond APOE

    Presenilins are membrane proteins with multiple transmembrane domains that are thought to contribute to the development of Alzheimer's disease by affecting the processing of beta-amyloid precursor protein.

  11. Deficiency of presenilin-1 inhibits the normal cleavage of amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1998-01-01 Risk genes beyond APOE

    Point mutations in the presenilin-1 gene (PS1) are a major cause of familial Alzheimer's disease.

  12. Frameshift mutants of beta amyloid precursor protein and ubiquitin-B in Alzheimer's and Down patients

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 1998-01-01 Down syndrome and Alzheimer's

    The cerebral cortex of Alzheimer's and Down syndrome patients is characterized by the presence of protein deposits in neurofibrillary tangles, neuritic plaques, and neuropil threads.

  13. Presenilin 1 is required for Notch1 and DII1 expression in the paraxial mesoderm

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1997-05-01 Risk genes beyond APOE

    Approximately 10% of cases of Alzheimer's disease are familial and associated with autosomal dominant inheritance of mutations in genes encoding the amyloid precursor protein, presenilin 1 (PS1) and presenilin 2 (PS2).

  14. Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid beta-protein in both transfected cells and transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature medicine 1997-01-01 Risk genes beyond APOE

    The mechanism by which mutations in the presenilin (PS) genes cause the most aggressive form of early-onset Alzheimer's disease (AD) is unknown, but fibroblasts from mutation carriers secrete increased levels of the amyloidogenic A beta 42 peptide, the main component of AD plaques.

  15. Increased amyloid-beta42(43) in brains of mice expressing mutant presenilin 1

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1996-10-01 Risk genes beyond APOE

    Mutations in the genes encoding amyloid-beta precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) are known to cause early-onset, autosomal dominant Alzheimer's disease.

  16. Assembly of microtubule-associated protein tau into Alzheimer-like filaments induced by sulphated glycosaminoglycans

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1996-10-01 Brain tissue and pathology

    The paired helical filament (PHF) is the major component of the neurofibrillary deposits that form a defining neuropathological characteristic of Alzheimer's disease.

  17. Apoptosis and increased generation of reactive oxygen species in Down's syndrome neurons in vitro

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1995-12-01 Down syndrome and Alzheimer's

    Down's syndrome (DS) or trisomy 21 is the most common genetic cause of mental retardation.

  18. Facilitation of lin-12-mediated signalling by sel-12, a Caenorhabditis elegans S182 Alzheimer's disease gene

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1995-09-01 Drug development

    The lin-12 and glp-1 genes of Caenorhabditis elegans are members of the lin-12/Notch family of receptors for intercellular signals that specify cell fate.

  19. Rapid induction of Alzheimer A beta amyloid formation by zinc

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 1994-09-01 Tau biomarkers

    A beta 1-40, a major component of Alzheimer's disease cerebral amyloid, is present in the cerebrospinal fluid and remains relatively soluble at high concentrations (less than or equal to 3.7 mM).

  20. Heightened synaptic plasticity of hippocampal CA1 neurons during a cholinergically induced rhythmic state

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1993-08-01 Disease mechanisms

    Brain cholinergic neurons are critical for memory function and their loss may contribute to memory impairment in Alzheimer's disease.

  21. Secretion of beta-amyloid precursor protein cleaved at the amino terminus of the beta-amyloid peptide

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1993-01-01 Tau biomarkers

    The accumulation in brain of senile plaques containing beta-amyloid protein (A beta) is a defining feature of Alzheimer's disease.

  22. Blood-brain barrier penetration and in vivo activity of an NGF conjugate

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 1993-01-01 Brain scans and imaging

    Nerve growth factor (NGF) is essential for the survival of both peripheral ganglion cells and central cholinergic neurons of the basal forebrain.

  23. Production of the Alzheimer amyloid beta protein by normal proteolytic processing

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 1992-10-01 Tau biomarkers

    The 4-kilodalton (39 to 43 amino acids) amyloid beta protein (beta AP), which is deposited as amyloid in the brains of patients with Alzheimer's diseases, is derived from a large protein, the amyloid beta protein precursor (beta APP).

  24. Targeting of cell-surface beta-amyloid precursor protein to lysosomes: alternative processing into amyloid-bearing fragments

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Nature 1992-06-01 Risk genes beyond APOE

    Progressive cerebral deposition of the amyloid beta-peptide is an early and invariant feature of Alzheimer's disease.

  25. A mutation in the amyloid precursor protein associated with hereditary Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Science (New York, N.Y.) 1991-10-01 Risk genes beyond APOE

    Alzheimer's disease is a form of localized amyloidosis characterized by cerebral cortical amyloid plaques, neurofibrillary tangles, and amyloid deposits within the walls of leptomeningeal vessels.

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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