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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. Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular neurodegeneration 2011-06-06 Disease mechanisms

    This study identifies tau oligomers as an acutely toxic tau species in vivo, and suggests that tau oligomers induce neurodegeneration by affecting mitochondrial and synaptic function, both of which are early hallmarks in AD and other tauopathies.

  2. β-carboline compounds, including harmine, inhibit DYRK1A and tau phosphorylation at multiple Alzheimer's disease-related sites

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2011-05-06 Down syndrome and Alzheimer's

    Harmine, a β-carboline alkaloid, is a high affinity inhibitor of the dual specificity tyrosine phosphorylation regulated kinase 1A (DYRK1A) protein.

  3. Dendritic spine pathology in neuropsychiatric disorders

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature neuroscience 2011-03-01 Brain tissue and pathology

    Substantial progress has been made toward understanding the genetic architecture, cellular substrates, brain circuits and endophenotypic profiles of neuropsychiatric disorders, including autism spectrum disorders (ASD), schizophrenia and Alzheimer's disease.

  4. APP processing in Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular brain 2011-01-07 Risk genes beyond APOE

    An important pathological feature of Alzheimer's disease (AD) is the presence of extracellular senile plaques in the brain.

  5. Huntington's disease: from molecular pathogenesis to clinical treatment

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. The Lancet. Neurology 2011-01-01 Mild cognitive impairment

    Huntington's disease is a progressive, fatal, neurodegenerative disorder caused by an expanded CAG repeat in the huntingtin gene, which encodes an abnormally long polyglutamine repeat in the huntingtin protein.

  6. Inhibition of GSK-3 ameliorates Abeta pathology in an adult-onset Drosophila model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PLoS genetics 2010-09-02 Drug development

    Abeta peptide accumulation is thought to be the primary event in the pathogenesis of Alzheimer's disease (AD), with downstream neurotoxic effects including the hyperphosphorylation of tau protein.

  7. Amyloid-beta-induced neuronal dysfunction in Alzheimer's disease: from synapses toward neural networks

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature neuroscience 2010-07-01 Disease mechanisms

    Alzheimer's disease is the most frequent neurodegenerative disorder and the most common cause of dementia in the elderly.

  8. An In Vitro Model for Neuroscience: Differentiation of SH-SY5Y Cells into Cells with Morphological and Biochemical Characteristics of Mature Neurons

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Alzheimer s Disease 2010-06-13 Disease mechanisms

    Neuroscience, including research on Alzheimer's disease, is hampered by the lack of suitable in vitro models to study the human nervous system.

  9. Inhibition of mTOR by rapamycin abolishes cognitive deficits and reduces amyloid-beta levels in a mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2010-04-01 Disease mechanisms

    Our data suggest that inhibition of mTOR by rapamycin, an intervention that extends lifespan in mice, can slow or block AD progression in a transgenic mouse model of the disease.

  10. Amyloid-beta as a positive endogenous regulator of release probability at hippocampal synapses

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature neuroscience 2009-12-01 Disease mechanisms

    Accumulation of cerebral amyloid-beta peptide (Abeta) is essential for developing synaptic and cognitive deficits in Alzheimer's disease.

  11. Adenosine A2AReceptor Blockade Prevents Synaptotoxicity and Memory Dysfunction Caused by β-Amyloid Peptides via p38 Mitogen-Activated Protein Kinase Pathway

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Neuroscience 2009-11-25 Disease mechanisms

    Alzheimer's disease (AD) is characterized by memory impairment, neurochemically by accumulation of beta-amyloid peptide (namely Abeta(1-42)) and morphologically by an initial loss of nerve terminals.

  12. Mitochondrial dynamics--fusion, fission, movement, and mitophagy--in neurodegenerative diseases

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Human molecular genetics 2009-10-01 Disease mechanisms

    Neurons are metabolically active cells with high energy demands at locations distant from the cell body.

  13. The excitotoxin quinolinic acid induces tau phosphorylation in human neurons

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2009-07-22 Treatments

    Some of the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QA), are likely to play a role in the pathogenesis of Alzheimer's disease (AD).

  14. Recent developments in Alzheimer's disease therapeutics

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. BMC medicine 2009-02-19 Costs and economics

    Alzheimer's disease is a devastating neurological disorder that affects more than 37 million people worldwide.

  15. Impaired adult neurogenesis in the dentate gyrus of a triple transgenic mouse model of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2008-08-13 Biomarkers

    However, male 3xTg-AD mice demonstrated a further reduction in the production of new neurones from 9 months of age (73% decrease) and a complete depletion at 12 months, when compared to controls.

  16. Ultrasound enhanced delivery of molecular imaging and therapeutic agents in Alzheimer's disease mouse models

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. PloS one 2008-05-14 Treatments

    Alzheimer's disease is a neurodegenerative disorder typified by the accumulation of a small protein, beta-amyloid, which aggregates and is the primary component of amyloid plaques.

  17. Dimerization of the transmembrane domain of amyloid precursor proteins and familial Alzheimer's disease mutants

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. BMC neuroscience 2008-01-30 Biomarkers

    The dissociation constants are correlated to both the Abeta42/Abeta40 ratio and the mean age of disease onset in AD patients.

  18. The GSK3 hypothesis of Alzheimer's disease

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of neurochemistry 2007-12-18 Inflammation and the immune system

    Glycogen synthase kinase 3 (GSK3) is a constitutively active, proline-directed serine/threonine kinase that plays a part in a number of physiological processes ranging from glycogen metabolism to gene transcription.

  19. Peptide Conformation and Supramolecular Organization in Amylin Fibrils: Constraints from Solid-State NMR

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Biochemistry 2007-11-01 Risk factors

    The 37-residue amylin peptide, also known as islet amyloid polypeptide, forms fibrils that are the main peptide or protein component of amyloid that develops in the pancreas of type 2 diabetes patients.

  20. Fibril specific, conformation dependent antibodies recognize a generic epitope common to amyloid fibrils and fibrillar oligomers that is absent in prefibrillar oligomers

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Molecular neurodegeneration 2007-09-26 Risk factors

    Since the fibril specific antibodies are conformation dependent, sequence-independent, and recognize epitopes that are distinct from those present in prefibrillar oligomers, they may have broad utility for detecting and characterizing the accumulation of amyloid fibrils and fibrillar type oligomers in degenerative diseases.

  21. AGGRESCAN: a server for the prediction and evaluation of "hot spots" of aggregation in polypeptides

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. BMC bioinformatics 2007-02-27 How common it is

    By identifying aggregation-prone segments in proteins, AGGRESCAN http://bioinf.uab.es/aggrescan/ shall facilitate (i) the identification of possible therapeutic targets for anti-depositional strategies in conformational diseases and (ii) the anticipation of aggregation phenomena during storage or recombinant production of bioactive polypeptides or polypeptide sets.

  22. Proteomic Identification of Novel Proteins in Cortical Lewy Bodies

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Brain Pathology 2007-02-08 Genetics

    Lewy body (LB) inclusions are one of the pathological hallmarks of Parkinson's disease (PD) and dementia with Lewy bodies (DLB).

  23. Hereditary parkinsonism with dementia is caused by mutations in ATP13A2, encoding a lysosomal type 5 P-type ATPase

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Nature genetics 2006-09-10 Risk genes beyond APOE

    Neurodegenerative disorders such as Parkinson and Alzheimer disease cause motor and cognitive dysfunction and belong to a heterogeneous group of common and disabling disorders.

  24. Alzheimer's Disease-Like Tau Neuropathology Leads to Memory Deficits and Loss of Functional Synapses in a Novel Mutated Tau Transgenic Mouse without Any Motor Deficits

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. American Journal Of Pathology 2006-08-01 Disease mechanisms

    Tau transgenic mice are valuable models to investigate the role of tau protein in Alzheimer's disease and other tauopathies.

  25. Synapse Formation and Function Is Modulated by the Amyloid Precursor Protein

    ✓ Peer-reviewed alzhub usefulness score 40 out of 100. Journal of Neuroscience 2006-07-05 Disease mechanisms

    The amyloid precursor protein (APP) is critical in the pathogenesis of Alzheimer's disease.

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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