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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. The β-Secretase BACE1 in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Biological psychiatry 2020-02-13 Risk genes beyond APOE

    BACE1 (beta-site amyloid precursor protein cleaving enzyme 1) was initially cloned and characterized in 1999.

  2. Intracellular Calcium Dysregulation by the Alzheimer's Disease-Linked Protein Presenilin 2

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. International journal of molecular sciences 2020-01-24 Risk genes beyond APOE

    Alzheimer's disease (AD) is the most common form of dementia.

  3. Presenilin 1 Regulates Membrane Homeostatic Pathways that are Dysregulated in Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of Alzheimer's disease : JAD 2020 Risk genes beyond APOE

    Mutations in the PSEN1 gene, encoding presenilin 1 (PS1), are the most common cause of familial Alzheimer's disease (fAD).

  4. Peptide-Based Molecular Strategies To Interfere with Protein Misfolding, Aggregation, and Cell Degeneration

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Angewandte Chemie (International ed. in English) 2019-11-28 Treatments

    Protein misfolding into amyloid fibrils is linked to more than 40 as yet incurable cell- and neurodegenerative diseases such as Alzheimer's disease, Parkinson's disease, and type 2 diabetes.

  5. From EST to structure models for functional inference of APP, BACE1, PSEN1, PSEN2 genes

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Bioinformation 2019-10-31 Risk genes beyond APOE

    Successive oxidative stress and biochemical changes results in neuronal death and neuritic plaques growth in Alzheimer's disease (AD).

  6. Cryo-EM structure and polymorphism of Aβ amyloid fibrils purified from Alzheimer's brain tissue

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Nature communications 2019-10-29 Vascular contributions

    The formation of Aβ amyloid fibrils is a neuropathological hallmark of Alzheimer's disease and cerebral amyloid angiopathy.

  7. Familial Alzheimer's disease presenilin-2 mutants affect Ca2+ homeostasis and brain network excitability

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Aging clinical and experimental research 2019-10-12 Risk genes beyond APOE

    Alzheimer's disease (AD) is the most frequent cause of dementia in the elderly.

  8. Structural Insights into Curli CsgA Cross-β Fibril Architecture Inspire Repurposing of Anti-amyloid Compounds as Anti-biofilm Agents

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. PLoS pathogens 2019-08-30 Treatments

    Curli amyloid fibrils secreted by Enterobacteriaceae mediate host cell adhesion and contribute to biofilm formation, thereby promoting bacterial resistance to environmental stressors.

  9. A Large Panel of Isogenic APP and PSEN1 Mutant Human iPSC Neurons Reveals Shared Endosomal Abnormalities Mediated by APP β-CTFs, Not Aβ

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Neuron 2019-08-12 Genetics

    Familial Alzheimer's disease (fAD) results from mutations in the amyloid precursor protein (APP) and presenilin (PSEN1 and PSEN2) genes.

  10. A novel V272D presenilin mutation associated with logopenia, disorientation, and apraxia in an autosomal-dominant Alzheimer's disease family

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurobiology of aging 2019-08-07 Biomarkers

    In the present study, a novel mutation in the presenilin 1 gene was discovered in an Iraq-native patient with early-onset Alzheimer's disease, who presented with speech impairment and memory decline at age 46 years.

  11. In search of pathogenic amyloid β-peptide in familial Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Progress in molecular biology and translational science 2019-07-13 Risk genes beyond APOE

    Early-onset familial Alzheimer's disease (FAD) is pathologically and clinically similar to the more common late-onset sporadic form of the disease.

  12. Associations of Neprilysin Activity in CSF with Biomarkers for Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neuro-degenerative diseases 2019-07-02 Tau biomarkers

    CSF-NEP was significantly inversely associated with CSF-Aβ42 and positively with the extent of neuronal injury as measured by CSF-tau and FDG-PET.

  13. Familial Alzheimer's disease patient-derived neurons reveal distinct mutation-specific effects on amyloid beta

    ✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular psychiatry 2019-04-12 Biomarkers

    Familial Alzheimer's disease (fAD) mutations alter amyloid precursor protein (APP) cleavage by γ-secretase, increasing the proportion of longer amyloidogenic amyloid-β (Aβ) peptides.

  14. Increased H-Bond Stability Relates to Altered ε-Cleavage Efficiency and Aβ Levels in the I45T Familial Alzheimer's Disease Mutant of APP

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Scientific reports 2019-03-29 Biomarkers

    Cleavage of the amyloid precursor protein's (APP) transmembrane domain (TMD) by γ-secretase is a crucial step in the aetiology of Alzheimer's Disease (AD).

  15. BACE-1 and γ-Secretase as Therapeutic Targets for Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Pharmaceuticals (Basel, Switzerland) 2019-03-19 Treatments

    Alzheimer's disease (AD) is a growing global health concern with a massive impact on affected individuals and society.

  16. Iron treatment inhibits Aβ42 deposition in vivo and reduces Aβ42/Aβ40 ratio

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Biochemical and biophysical research communications 2019-02-18 Biomarkers

    Alzheimer's disease (AD) is characterized by the formation of extracellular amyloid plaques containing the amyloid β-protein (Aβ) within the parenchyma of the brain.

  17. A cellular complex of BACE1 and γ-secretase sequentially generates Aβ from its full-length precursor

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. The Journal of cell biology 2019-01-09 Biomarkers

    Intramembrane proteolysis of transmembrane substrates by the presenilin-γ-secretase complex is preceded and regulated by shedding of the substrate's ectodomain by α- or β-secretase.

  18. Small-molecule induction of Aβ-42 peptide production in human cerebral organoids to model Alzheimer's disease associated phenotypes

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. PloS one 2018-12-17 Biomarkers

    Human mini-brains (MB) are cerebral organoids that recapitulate in part the complexity of the human brain in a unique three-dimensional in vitro model, yielding discrete brain regions reminiscent of the cerebral cortex.

  19. A new era for understanding amyloid structures and disease

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Nature reviews. Molecular cell biology 2018-12-01 Risk factors

    The aggregation of proteins into amyloid fibrils and their deposition into plaques and intracellular inclusions is the hallmark of amyloid disease.

  20. Modeling amyloid beta and tau pathology in human cerebral organoids

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Molecular psychiatry 2018-08-31 Down syndrome and Alzheimer's

    The typical abnormalities observed in the brain of Alzheimer's disease (AD) patients include synaptic alterations, neuronal death, brain inflammation, and the accumulation of protein aggregates in the form of amyloid plaques and neurofibrillary tangles.

  21. Amyloid toxicity in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Reviews in the neurosciences 2018-08-01 End-of-life care

    A major feature of Alzheimer's disease (AD) pathology is the plaque composed of aggregated amyloid-β (Aβ) peptide.

  22. Cognitive and emotional alterations in App knock-in mouse models of Aβ amyloidosis

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. BMC neuroscience 2018-07-28 Biomarkers

    App NL/NL and App NL-G-F/NL-G-F mice exhibit behavioral changes associated with non-cognitive, emotional domains before the onset of definitive cognitive deficits.

  23. Epileptic seizures in autosomal dominant forms of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Seizure 2018-07-19 Risk genes beyond APOE

    Alzheimer's disease (AD) is a heterogeneous neurodegenerative disorder and represents the most common form of dementia in the elderly.

  24. Adipose-derived stem cells (ADSC) have a therapeutic potential for the treatment of neurodegenerative disorders such as Alzheimer's disease (AD).

  25. 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.

  26. Differential Effects of Alzheimer's Disease Aβ40 and 42 on Endocytosis and Intraneuronal Trafficking

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neuroscience 2018-01-11 Biomarkers

    Anomalous neuronal accumulation of Aβ peptides was shown to affect synaptic transmission and contribute to neurodegeneration in Alzheimer's disease (AD) brain.

  27. The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Journal of Alzheimer's disease : JAD 2018-01-01 Brain tissue and pathology

    The amyloid-β oligomer (AβO) hypothesis was introduced in 1998.

  28. β-Sheet Structure within the Extracellular Domain of C99 Regulates Amyloidogenic Processing

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Scientific reports 2017-12-07 Biomarkers

    Familial mutations in C99 can increase the total level of the soluble Aβ peptides produced by proteolysis, as well as the Aβ42/Aβ40 ratio, both of which are linked to the progression of Alzheimer's disease.

  29. APP mouse models for Alzheimer's disease preclinical studies

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. The EMBO journal 2017-08-01 Risk genes beyond APOE

    Animal models of human diseases that accurately recapitulate clinical pathology are indispensable for understanding molecular mechanisms and advancing preclinical studies.

  30. 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.

  31. 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.

  32. 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.

  33. ErbB2 regulates autophagic flux to modulate the proteostasis of APP-CTFs in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2017-03-28 Disease mechanisms

    Proteolytic processing of amyloid precursor protein (APP) C-terminal fragments (CTFs) by γ-secretase underlies the pathogenesis of Alzheimer's disease (AD).

  34. Pathogenic PS1 phosphorylation at Ser367

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. eLife 2017-01-30 Biomarkers

    The high levels of serine (S) and threonine (T) residues within the Presenilin 1 (PS1) N-terminus and in the large hydrophilic loop region suggest that the enzymatic function of PS1/γ-secretase can be modulated by its 'phosphorylated' and 'dephosphorylated' states.

  35. The Amyloid Cascade Hypothesis in Alzheimer's Disease: It's Time to Change Our Mind

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Current neuropharmacology 2017-01-01 Treatments

    Since its discovery in 1984, the beta amyloid peptide has treaded the boards of neurosciences as the star molecule in Alzheimer's disease pathogenesis.

  36. Analysis of 138 pathogenic mutations in presenilin-1 on the in vitro production of Aβ42 and Aβ40 peptides by γ-secretase

    ✓ Peer-reviewed alzhub usefulness score 41 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2016-12-05 Biomarkers

    A hallmark of Alzheimer's disease (AD) is the aggregation of β-amyloid peptides (Aβ) into amyloid plaques in patient brain.

  37. Amyloid tracers binding sites in autosomal dominant and sporadic Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. Alzheimer's & dementia : the journal of the Alzheimer's Association 2016-09-28 Brain scans and imaging

    3H-PIB, 3H-florbetaben, 3H-AZD2184, and BTA-1 shared a high- and a varying low-affinity binding site in the frontal cortex of sporadic AD.

  38. Self-Organizing 3D Human Neural Tissue Derived from Induced Pluripotent Stem Cells Recapitulate Alzheimer’s Disease Phenotypes

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PLoS ONE 2016-09-13 Risk genes beyond APOE

    The dismal success rate of clinical trials for Alzheimer's disease (AD) motivates us to develop model systems of AD pathology that have higher predictive validity.

  39. Alzheimer's disease-associated mutations increase amyloid precursor protein resistance to γ-secretase cleavage and the Aβ42/Aβ40 ratio

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Cell discovery 2016-08-23 Biomarkers

    Mutations in the amyloid precursor protein (APP) gene and the aberrant cleavage of APP by γ-secretase are associated with Alzheimer's disease (AD).

  40. Atomic-resolution structure of a disease-relevant Aβ(1-42) amyloid fibril

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2016-07-28 Risk genes beyond APOE

    Amyloid-β (Aβ) is present in humans as a 39- to 42-amino acid residue metabolic product of the amyloid precursor protein.

  41. Atomic Resolution Structure of Monomorphic Aβ42 Amyloid Fibrils

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Journal of the American Chemical Society 2016-07-14 Risk genes beyond APOE

    Amyloid-β (Aβ) is a 39-42 residue protein produced by the cleavage of the amyloid precursor protein (APP), which subsequently aggregates to form cross-β amyloid fibrils that are a hallmark of Alzheimer's disease (AD).

  42. 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.

  43. Proteolytic processing of Neuregulin-1

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research bulletin 2016-07-05 Treatments

    Neuregulin-1 (NRG1), known also as heregulin, acetylcholine receptor inducing activity (ARIA), glial growth factor (GGF), or sensory and motor neuron derived factor (SMDF), is a key factor for many developmental processes and in adult brain.

  44. P1‐146: Chlamydia Pneumoniae‐Infected Astrocytes Alter Their Expression of Adam10, Bace1, and Presenilin‐1 Proteases

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Alzheimer s & Dementia 2016-07-01 Risk genes beyond APOE

    Utilizing β-amyloid precursor protein (βAPP) as a substrate, α-, β-, and γ-secretases are responsible for sequential cleavage events leading to the formation of β-amyloid, the classic pathologic hallmark of Alzheimer’s Disease.

  45. Alzheimer's disease due to loss of function: A new synthesis of the available data

    ✓ Peer-reviewed alzhub usefulness score 57 out of 100. Progress in neurobiology 2016-06-18 Biomarkers

    Alzheimer's Disease (AD) is a highly complex disease involving a broad range of clinical, cellular, and biochemical manifestations that are currently not understood in combination.

  46. 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).

  47. The role of calsyntenin-3 in dystrophic neurite formation in Alzheimer's disease brain

    ✓ Peer-reviewed alzhub usefulness score 38 out of 100. Geriatrics & gerontology international 2016-03 Disease mechanisms

    β-Amyloid (Aβ) oligomers may play an important role in the early pathogenesis of Alzheimer's disease: cognitive impairment caused by synaptic dysfunction.

  48. Amyloid cascade in Alzheimer's disease: Recent advances in medicinal chemistry

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. European journal of medicinal chemistry 2016-02-22 Treatments

    Alzheimer's disease is of major concern all over the world due to a number of factors including (i) an aging population (ii) increasing life span and (iii) lack of effective pharmacotherapy options.

  49. Sampling the conformational space of the catalytic subunit of human γ-secretase

    ✓ Peer-reviewed alzhub usefulness score 43 out of 100. eLife 2015-12-01 Risk genes beyond APOE

    Human γ-secretase is an intra-membrane protease that cleaves many different substrates.

  50. Laser-scanning confocal microscopy, flow cytometry analysis and inductively coupled plasma-atomic emission spectroscopy ICP-AES revealed high cellular uptake of B6-SA-SeNPs by cerebral endothelial cells (bEnd.3).

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.

All topic tags with their study counts