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Newest in this topic

  1. Precision Nanocrystal Theranostics for Neurodegenerative Proteopathies: Strategies to Cross the Blood-Brain Barrier and Target Protein Aggregation 2026-10-26
  2. Temporal Proteomics Links the APP London Mutation to Early Cholesterol Remodeling Cell Programs in Human Neurons 2026-10-24
  3. Stimulating microglial neuroinflammation with amyloid-beta oligomers compatible with solid-state NMR structural characterization 2026-10-20

Studies

343 studies carry this tag.

Date range

1985 to 2026

Top journals

  • Proceedings of the National Academy of Sciences of the United States of America 35
  • Nature 23
  • Neuron 14
  • The Journal of biological chemistry 14
  • Science (New York, N.Y.) 12

147 journals in all.

Newest first, then by address. Each study has a usefulness score out of 100 (rubric version 4.0); tap a score to see what makes it up. Tags were assigned automatically from each study's title and summary. The same studies as a filter in the library.

  1. Amyloidosis: a convoluted story

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. British Journal of Haematology 2001-09-01 Drug development

    However, the fibrils in primary amyloidosis (AL) consist of the variable portion of a monoclonal light chain (κ or λ); secondary amyloidosis (AA) fibrils consist of protein A, a non-immunoglobulin; familial amyloidosis fibrils are usually composed of mutated transthyretin (prealbumin); senile systemic amyloid fibrils consist of normal transthyretin; and amyloid associated with long-term dialysis consists of β2-microglobulin.

  2. Cholesterol and Alzheimer's disease: is there a link?

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neurology 2001-09-01 Drug development

    The Abeta-amyloid peptide (Abeta), the main component of amyloid plaques, is derived by proteolytic cleavage from the amyloid precursor protein (APP).

  3. The 'Arctic' APP mutation (E693G) causes Alzheimer's disease by enhanced Abeta protofibril formation

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature neuroscience 2001-09-01 Risk genes beyond APOE

    Several pathogenic Alzheimer's disease (AD) mutations have been described, all of which cause increased amyloid beta-protein (Abeta) levels.

  4. Immune hyporesponsiveness to amyloid beta-peptide in amyloid precursor protein transgenic mice: implications for the pathogenesis and treatment of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2001-08-21 Down syndrome and Alzheimer's

    Alzheimer's disease is a dementia that involves progressive deposition of amyloid beta-protein (Abeta) in brain regions important for memory and cognition, followed by secondary inflammation that contributes to the neuropathologic process.

  5. Nicastrin binds to membrane-tethered Notch

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Nature cell biology 2001-08-01 Drug development

    The presenilins and nicastrin, a type 1 transmembrane glycoprotein, form high molecular weight complexes that are involved in cleaving the beta-amyloid precursor protein (betaAPP) and Notch in their transmembrane domains.

  6. Treatment with a copper-zinc chelator markedly and rapidly inhibits beta-amyloid accumulation in Alzheimer's disease transgenic mice

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Neuron 2001-06-01 Biomarkers

    Inhibition of neocortical beta-amyloid (Abeta) accumulation may be essential in an effective therapeutic intervention for Alzheimer's disease (AD).

  7. Low cholesterol stimulates the nonamyloidogenic pathway by its effect on the alpha -secretase ADAM 10

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2001-04-17 Risk genes beyond APOE

    Biochemical, epidemiological, and genetic findings demonstrate a link between cholesterol levels, processing of the amyloid precursor protein (APP), and Alzheimer's disease.

  8. Early-onset amyloid deposition and cognitive deficits in transgenic mice expressing a double mutant form of amyloid precursor protein 695

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 2001-03-15 Risk genes beyond APOE

    We have created early-onset transgenic (Tg) models by exploiting the synergistic effects of familial Alzheimer's disease mutations on amyloid beta-peptide (Abeta) biogenesis.

  9. Functional gamma-secretase inhibitors reduce beta-amyloid peptide levels in brain

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurochemistry 2001-01-01 Risk genes beyond APOE

    Converging lines of evidence implicate the beta-amyloid peptide (Ass) as causative in Alzheimer's disease.

  10. 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).

  11. Clearance of Alzheimer's amyloid-ss(1-40) peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of clinical investigation 2000-12-01 Genetics

    Elimination of amyloid-ss peptide (Ass) from the brain is poorly understood.

  12. beta amyloid protein (Abeta) is a 40-43 amino acid peptide derived from amyloid precursor protein (APP).

  13. Neuron-specific phosphorylation of Alzheimer's beta-amyloid precursor protein by cyclin-dependent kinase 5

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of neurochemistry 2000-09-01 Drug development

    The mature form of Alzheimer's beta-amyloid precursor protein (APP) is phosphorylated specifically at Thr(668) in neurons.

  14. Hypercholesterolemia accelerates the Alzheimer's amyloid pathology in a transgenic mouse model

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of disease 2000-08-01 Risk genes beyond APOE

    Recent data suggest that cholesterol metabolism is linked to susceptibility to Alzheimer's disease (AD).

  15. 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.

  16. Human aspartic protease memapsin 2 cleaves the beta-secretase site of beta-amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2000-02-01 Risk genes beyond APOE

    The cDNAs of two new human membrane-associated aspartic proteases, memapsin 1 and memapsin 2, have been cloned and sequenced.

  17. Intraneuronal Abeta42 accumulation in human brain

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The American journal of pathology 2000-01-01 Risk genes beyond APOE

    Alzheimer's disease (AD) is characterized by the deposition of senile plaques (SPs) and neurofibrillary tangles (NFTs) in vulnerable brain regions.

  18. Apolipoprotein E is essential for amyloid deposition in the APP V717F transgenic mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Proceedings of the National Academy of Sciences 1999-12-21 Genetics

    We quantified the amount of amyloid beta-peptide (Abeta) immunoreactivity as well as amyloid deposits in a large cohort of transgenic mice overexpressing the V717F human amyloid precursor protein (APP(V717F+/-) TG mice) with no, one, or two mouse apolipoprotein E (Apoe) alleles at various ages.

  19. Identification of a novel aspartic protease (Asp 2) as beta-secretase

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Molecular and cellular neurosciences 1999-12-01 Risk genes beyond APOE

    The Alzheimer's disease beta-amyloid peptide (Abeta) is produced by excision from the type 1 integral membrane glycoprotein amyloid precursor protein (APP) by the sequential actions of beta- and then gamma-secretases.

  20. 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.

  21. 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.

  22. Constitutive and regulated alpha-secretase cleavage of Alzheimer's amyloid precursor protein by a disintegrin metalloprotease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-03-01 Risk genes beyond APOE

    Amyloid beta peptide (Abeta), the principal proteinaceous component of amyloid plaques in brains of Alzheimer's disease patients, is derived by proteolytic cleavage of the amyloid precursor protein (APP).

  23. Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1999-03-01 Disease mechanisms

    Transgenic mice overexpressing different forms of amyloid precursor protein (APP), i.e. wild type or clinical mutants, displayed an essentially comparable early phenotype in terms of behavior, differential glutamatergic responses, deficits in maintenance of long term potentiation, and premature death.

  24. Evidence for a physical interaction between presenilin and Notch

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-03-01 Drug development

    Genetic analyses in Caenorhabditis elegans demonstrate that sel-12 and hop-1, homologues of the Alzheimer's disease-associated presenilin genes, modify signaling through LIN-12 and GLP-1, homologues of the Notch cell surface receptor.

  25. Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-03-01 Risk genes beyond APOE

    Autosomal dominant forms of familial Alzheimer's disease (FAD) are associated with increased production of the amyloid beta peptide, Abeta42, which is derived from the amyloid protein precursor (APP).

  26. Insulin-degrading enzyme regulates extracellular levels of amyloid beta-protein by degradation

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1998-12-01 Tau biomarkers

    Excessive cerebral accumulation of the 42-residue amyloid beta-protein (Abeta) is an early and invariant step in the pathogenesis of Alzheimer's disease.

  27. Interaction of cytosolic adaptor proteins with neuronal apolipoprotein E receptors and the amyloid precursor protein

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1998-12-01 Genetics

    Apolipoprotein E, alpha2-macroglobulin, and amyloid precursor protein (APP) are involved in the development of Alzheimer's disease.

  28. 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.

  29. 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).

  30. 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.

  31. 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).

  32. 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.

  33. 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.

  34. 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).

  35. 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).

  36. 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.

  37. 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.

  38. 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.

  39. 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.

  40. 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.

  41. 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.

  42. 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.

  43. 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.

  44. 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).

  45. Analysis of heterogeneous A4 peptides in human cerebrospinal fluid and blood by a newly developed sensitive Western blot assay

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of biological chemistry 1996-09-01 Tau biomarkers

    The betaA4 peptide, a major component of senile plaques in Alzheimer's disease (AD) brain, has been found in cerebrospinal fluid (CSF) and blood of both AD patients and normal subjects.

  46. 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.

  47. Induction of neuroprotective kappa B-dependent transcription by secreted forms of the Alzheimer's beta-amyloid precursor

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research. Molecular brain research 1996-08-01 Drug development

    A significant fraction of the beta-amyloid precursor protein is proteolytically processed to yield large secreted forms (sAPP).

  48. 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.

  49. Acetylcholinesterase accelerates assembly of amyloid-beta-peptides into Alzheimer's fibrils: possible role of the peripheral site of the enzyme

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 1996-04-01 Disease mechanisms

    Acetylcholinesterase (AChE), an important component of cholinergic synapses, colocalizes with amyloid-beta peptide (A beta) deposits of Alzheimer's brain.

  50. 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.

From across this tag

10 of the 343 studies in this tag, 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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