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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. 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.

  2. Presynaptic endocytic factors in autophagy and neurodegeneration

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Current opinion in neurobiology 2018-01-06 Disease mechanisms

    Neuronal signaling depends on the exocytic fusion and subsequent endocytic retrieval and reformation of neurotransmitter-containing synaptic vesicles at synapses.

  3. A refined concept: α-synuclein dysregulation disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurochemistry international 2018-01-02 Brain tissue and pathology

    α-synuclein (αSyn) still remains a mysterious protein even two decades after SNCA encoding it was identified as the first causative gene of familial Parkinson's disease (PD).

  4. Differences in Synaptic Dysfunction Between rTg4510 and APP/PS1 Mouse Models of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Journal of Alzheimer's disease : JAD 2018 Disease mechanisms

    Genetically modified mice have provided insights into the progression and pathology of Alzheimer's disease (AD).

  5. Tau-mediated Neurodegeneration and Potential Implications in Diagnosis and Treatment of Alzheimer's Disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Chinese medical journal 2017-12-20 Drug development

    Amyloid plaques enriched with extracellular amyloid beta (Aβ) and intracellular neurofibrillary tangles comprised of hyperphosphorylated tau proteins are the two main pathological hallmarks of AD.

  6. 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.

  7. "Tau immunotherapy: Hopes and hindrances"

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Human vaccines & immunotherapeutics 2017-12-01 Drug development

    Alzheimer's disease (AD) is a progressive neurological disorder having two major pathological hallmarks: the extracellular senile plaques and intracellular neurofibrillary tangles composed of amyloid beta protein and hyperphosphorylated tau respectively.

  8. Neurodegeneration and the ordered assembly of α-synuclein

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cell and tissue research 2017-11-08 Brain tissue and pathology

    In 2017, it was 200 years since James Parkinson published 'An Essay on the Shaking Palsy' and 20 years since α-synuclein aggregation came to the fore.

  9. Near infrared light decreases synaptic vulnerability to amyloid beta oligomers

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Scientific reports 2017-11-08 Disease mechanisms

    Synaptic dysfunction due to the disrupting binding of amyloid beta (Aβ) and tau oligomers is one of the earliest impairments in Alzheimer's Disease (AD), driving initial cognitive deficits and clinical manifestation.

  10. β-Amyloid and the Pathomechanisms of Alzheimer's Disease: A Comprehensive View

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecules (Basel, Switzerland) 2017-10-10 Disease mechanisms

    Protein dyshomeostasis is the common mechanism of neurodegenerative diseases such as Alzheimer's disease (AD).

  11. Receptors make the pathway choice for protein degradation

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Autophagy 2017-08-10 Disease mechanisms

    Damaged or aggregated proteins and organelles accumulate with age and contribute to various age-related pathologies including Alzheimer, Parkinson or Huntington diseases.

  12. Mitophagy in neurodegenerative diseases

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurochemistry international 2017-08-08 Disease mechanisms

    Neurodegenerative diseases, such as Parkinson's disease (PD), Alzheimer's disease (AD), Huntington's disease (HD), and Amyotrophic Lateral Sclerosis (ALS), are a complex "family" of pathologies, characterised by the progressive loss of neurons and/or neuronal functions, leading to severe physical and cognitive inabilities in affected patients.

  13. Amyloid-β Peptide Is Needed for cGMP-Induced Long-Term Potentiation and Memory

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2017-06-16 Disease mechanisms

    High levels of amyloid-β peptide (Aβ) have been related to Alzheimer's disease pathogenesis.

  14. Regulation of postsynaptic signaling in structural synaptic plasticity

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Current opinion in neurobiology 2017-06-07 Disease mechanisms

    Morphological changes of dendritic spines are strongly associated with synaptic development and synaptic plasticity, which underlies learning and memory.

  15. Emerging amyloid and tau targeting treatments for Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Expert review of neurotherapeutics 2017-05-19 Drug development

    With an ageing global population, the number of people with dementia, and its main cause Alzheimer's disease (AD), is growing. current licensed treatments available for ad are only alleviate the symptoms of the disease, and are effective only in some people with ad for a limited time. there are currently no therapies that target the disease process.

  16. Tau at the Crossroads between Neurotoxicity and Neuroprotection

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neuron 2017-05-17 Drug development

    In contrast to the idea that tau phosphorylation is toxic, Ittner et al. (2016) recently showed that specific tau phosphorylation is neuroprotective, phenocopying tau ablation (DeVos et al., 2017), thus highlighting the complex tau biology that underlies neurotoxicity and neuroprotection.

  17. Protein Quality Control and the Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Continuum

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Frontiers in molecular neuroscience 2017-05-10 Disease mechanisms

    Protein homeostasis, or proteostasis, has an important regulatory role in cellular function.

  18. Tau Positron Emission Tomography Imaging

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cold Spring Harbor perspectives in biology 2017-05-01 Brain scans and imaging

    Alzheimer's disease (AD) is a chronic neurodegenerative disorder and the most common cause of dementia among the elderly population.

  19. Lewy Body Disorders

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Neurologic clinics 2017-05 Brain tissue and pathology

    Dementia syndromes associated with Lewy bodies are subdivided into dementia with Lewy bodies (DLB), an underdiagnosed cause of dementia in the elderly, and Parkinson disease with dementia (PDD), cognitive impairment appearing in people diagnosed with Parkinson disease.

  20. Synaptic Dysfunction in Alzheimer's Disease: Aβ, Tau, and Epigenetic Alterations

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Molecular neurobiology 2017-04-29 Disease mechanisms

    Alzheimer's disease (AD) is a complex neurodegenerative disorder characterized in the early stages by loss of learning and memory.

  21. Netrin-1 improves the amyloid-β-mediated suppression of memory and synaptic plasticity

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Brain research bulletin 2017-04-04 Disease mechanisms

    The aim of this study was to investigate the effects of netrin-1 (NT-1) on amyloid-beta (Aβ)-induced impairments in learning-memory and synaptic plasticity.

  22. Control of mitochondrial biogenesis and function by the ubiquitin-proteasome system

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Open biology 2017-04 Disease mechanisms

    Mitochondria are pivotal organelles in eukaryotic cells.

  23. Altered Synapse Stability in the Early Stages of Tauopathy

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cell reports 2017-03-28 Disease mechanisms

    Synapse loss is a key feature of dementia, but it is unclear whether synaptic dysfunction precedes degenerative phases of the disease.

  24. 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).

  25. Regulation of Cognitive Processing by Hippocampal Cholinergic Tone

    ✓ Peer-reviewed alzhub usefulness score 39 out of 100. Cerebral cortex (New York, N.Y. : 1991) 2017-02-01 Disease mechanisms

    Cholinergic dysfunction has been associated with cognitive abnormalities in a variety of neurodegenerative and neuropsychiatric diseases.

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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