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Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.

Download bibliography of all 1,352 studies, highest score first: BibTeX (.bib) · RIS (.ris)

Highest usefulness score first. Studies without a score come last.

  1. Gamma-secretase is a membrane protein complex comprised of presenilin, nicastrin, Aph-1, and Pen-2

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2003-05-09 Risk genes beyond APOE

    gamma-Secretase catalyzes the intramembrane proteolysis of Notch, beta-amyloid precursor protein, and other substrates as part of a new signaling paradigm and as a key step in the pathogenesis of Alzheimer's disease.

  2. Reconstitution of gamma-secretase activity

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Nature cell biology 2003-05-01 Risk genes beyond APOE

    gamma-Secretase is a membrane protein complex with an unusual aspartyl protease activity that catalyses the regulated intramembranous cleavage of the beta-amyloid precursor protein (APP) to release the Alzheimer's disease (AD)-associated amyloid beta-peptide (Abeta) and the APP intracellular domain (AICD).

  3. Roles of amyloid precursor protein and its fragments in regulating neural activity, plasticity and memory

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Progress in neurobiology 2003-05-01 Disease mechanisms

    Indeed, it has been proposed that reductions in the level or activity of certain APP fragments, in addition to accumulation of Abeta, may play a critical role in the cognitive dysfunction associated with AD, particularly early in the course of the disease.

  4. Aph-1, Pen-2, and Nicastrin with Presenilin generate an active gamma-Secretase complex

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2003-04-01 Risk genes beyond APOE

    Gamma-Secretase cleaves the Amyloid Precursor Protein (APP) in its transmembrane domain, releasing the amyloid peptide Abeta.

  5. MAPKs: new targets for neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Expert opinion on therapeutic targets 2003-04-01 End-of-life care

    Neurodegenerative diseases remain a huge unmet pharmaceutical need.

  6. The metallobiology of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Trends in neurosciences 2003-04-01 How common it is

    The cause of Alzheimer's disease (AD) is closely related to the aggregation of a normal protein, beta-amyloid (Abeta), within the neocortex.

  7. APP processing and synaptic function

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuron 2003-03-01 Risk genes beyond APOE

    A large body of evidence has implicated Abeta peptides and other derivatives of the amyloid precursor protein (APP) as central to the pathogenesis of Alzheimer's disease (AD).

  8. beta-Amyloid aggregation induced by human acetylcholinesterase: inhibition studies

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Biochemical pharmacology 2003-02-01 Treatments

    The aggregation of beta-amyloid (1-40) (Abeta) induced by human recombinant acetylcholinesterase (HuAChE) was studied by means of circular dichroism (CD) and by thioflavin T fluorescence spectroscopy.

  9. Frontal cortex BDNF levels correlate with working memory in an animal model of Down syndrome

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Behavioural brain research 2003-02-01 Down syndrome and Alzheimer's

    Individuals with Down syndrome (DS) develop most neuropathological hallmarks of Alzheimer's disease early in life, including loss of cholinergic markers in the basal forebrain.

  10. Involvement of oxidative stress in the enhancement of acetylcholinesterase activity induced by amyloid beta-peptide

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience research 2003-01-01 Brain scans and imaging

    Acetylcholinesterase (AChE) activity is increased within and around amyloid plaques, which are present in Alzheimer's disease (AD) patient's brain.

  11. Efflux of human and mouse amyloid beta proteins 1-40 and 1-42 from brain: impairment in a mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience 2003-01-01 Drug development

    Brain to blood transport is believed to be a major determinant of the amount of amyloid beta protein (AbetaP) found in brain.

  12. Lipid rafts: structure, function and role in HIV, Alzheimer's and prion diseases

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Expert Reviews in Molecular Medicine 2002-12-20 Drug development

    The fluid mosaic model of the plasma membrane has evolved considerably since its original formulation 30 years ago.

  13. Neuroprotection by memantine against neurodegeneration induced by beta-amyloid(1-40)

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research 2002-12-01 Biomarkers

    Progressive neuronal loss and cognitive decline in Alzheimer's disease (AD) might be aggravated by beta-amyloid-enhanced excitotoxicity.

  14. Amyloid beta-peptide (1-42)-induced oxidative stress and neurotoxicity: implications for neurodegeneration in Alzheimer's disease brain. A review

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Free radical research 2002-12-01 Genetics

    Brain membranes from human apoE4 mice have greater vulnerability to Abeta(1-42)-induced oxidative stress than brain membranes from apoE2 or E3, assessed by the same indices, consistent with the notion of a coupling of the oxidative environment in AD brain and increased risk of developing this disorder.

  15. Molecular targeting of Alzheimer's amyloid plaques for contrast-enhanced magnetic resonance imaging

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of disease 2002-11-01 Treatments

    Smart molecular probes for both diagnostic and therapeutic purposes are expected to provide significant advances in clinical medicine and biomedical research.

  16. Amyloid-beta induces Smac release via AP-1/Bim activation in cerebral endothelial cells

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2002-11-01 Drug development

    Insoluble fibrils of amyloid-beta peptide (Abeta) are the major component of senile and vascular plaques found in the brains of Alzheimer's disease (AD) patients.

  17. Amyloid beta -peptide inhibition of the PKA/CREB pathway and long-term potentiation: reversibility by drugs that enhance cAMP signaling

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2002-09-20 Disease mechanisms

    Changes in hippocampal function seem critical for cognitive impairment in Alzheimer's disease (AD).

  18. Evidence that amyloid beta-peptide-induced lipid peroxidation and its sequelae in Alzheimer's disease brain contribute to neuronal death

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neurobiology of aging 2002-09-01 Genetics

    Abeta(1-42) addition to synaptosomes also results in HNE binding to Glt-1, thereby coupling increased Abeta(1-42) in AD brain to increased lipid peroxidation and its sequelae and possibly explaining the mechanism of glutamate transport inhibition known in AD brain.

  19. Alzheimer's disease (AD) is a neurodegenerative disorder in which oxidative stress has been implicated as an important event in the progression of the pathology.

  20. The Alzheimer's A beta -peptide is deposited at sites of complement activation in pathologic deposits associated with aging and age-related macular degeneration

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2002-08-20 Brain scans and imaging

    Age-related macular degeneration (AMD) is a leading cause of irreversible vision loss in older individuals worldwide.

  21. Oxidative alterations of proteins by reactive oxygen species (ROS) have been implicated in the progression of aging and age-related neurodegenerative disorders such as Alzheimer's disease (AD).

  22. Dendritic spine pathology: cause or consequence of neurological disorders?

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Brain research. Brain research reviews 2002-06-01 Prevention and risk

    Altered dendritic spines are characteristic of traumatized or diseased brain.

  23. Intraneuronal Abeta42 accumulation in Down syndrome brain

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis 2002-06-01 Down syndrome and Alzheimer's

    Alzheimer's disease (AD) brains display A beta (Abeta) plaques, inflammatory changes and neurofibrillary tangles (NFTs).

  24. Aggregate-prone proteins with polyglutamine and polyalanine expansions are degraded by autophagy

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Human molecular genetics 2002-05-01 Disease mechanisms

    Protein conformational disorders (PCDs), such as Alzheimer's disease, Huntington's disease (HD), Parkinson's disease and oculopharyngeal muscular dystrophy, are associated with proteins that misfold and aggregate.

  25. Drebrin, a dendritic spine protein, is manifold decreased in brains of patients with Alzheimer's disease and Down syndrome

    ✓ Peer-reviewed alzhub usefulness score 36 out of 100. Neuroscience letters 2002-05-01 Down syndrome and Alzheimer's

    Drebrin, located in the dendritic spines of the neuron, plays a role in the synaptic plasticity together with actin filaments.

From across this topic

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