ReviewCellular and molecular life sciences : CMLS2011
Modes of Aβ toxicity in Alzheimer's disease.
Review in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
34 citing papers in PubMed, 83 citations in OpenAlex.
- Spore powder of Ganoderma lucidum for the treatment of Alzheimer disease: A pilot study.Medicine · 2018Trial
- Decoding the mechanisms of amyloid-β in synaptic toxicity.Journal of Alzheimer's disease : JAD · 2026Review
- Delta-9-tetrahydrocannabinol delineates D-galactose and aluminium chloride-induced cognitive dysfunction and neurodegeneration in the hippocampus of the Wistar rat model.Journal of biosciences · 2026Article
- Article
- Advancements in nasal drug delivery system of natural products.Frontiers in pharmacology · 2025Review
- The Contribution of the Renin-Angiotensin System to Alzheimer's Disease.Current topics in behavioral neurosciences · 2025Review
- Advances in the development paradigm of biosample-based biosensors for early ultrasensitive detection of alzheimer's disease.Journal of nanobiotechnology · 2021Review
- MicroRNA-107 Ameliorates Damage in a Cell Model of Alzheimer's Disease by Mediating the FGF7/FGFR2/PI3K/Akt Pathway.Journal of molecular neuroscience : MN · 2020Article
- Link between the unfolded protein response and dysregulation of mitochondrial bioenergetics in Alzheimer's disease.Cellular and molecular life sciences : CMLS · 2019Article
- TauNeuroscience · 2017Article
- Studying the Progression of Amyloid Pathology and Its Therapy Using Translational Longitudinal Model of Accumulation and Distribution of Amyloid Beta.CPT: pharmacometrics & systems pharmacology · 2017Article
- Tocotrienol Affects Oxidative Stress, Cholesterol Homeostasis and the Amyloidogenic Pathway in Neuroblastoma Cells: Consequences for Alzheimer's Disease.International journal of molecular sciences · 2016Article
- Tau physiology and pathomechanisms in frontotemporal lobar degeneration.Journal of neurochemistry · 2016Review
- Sex hormone-related neurosteroids differentially rescue bioenergetic deficits induced by amyloid-β or hyperphosphorylated tau protein.Cellular and molecular life sciences : CMLS · 2016Article
- Geniposide Protects Primary Cortical Neurons against Oligomeric Aβ1-42-Induced Neurotoxicity through a Mitochondrial Pathway.PloS one · 2016Article
- Curcumin and Apigenin - novel and promising therapeutics against chronic neuroinflammation in Alzheimer's disease.Neural regeneration research · 2015Review
- Evidence against a role of P-glycoprotein in the clearance of the Alzheimer's disease Aβ1-42 peptides.Cell stress & chaperones · 2015Article
- Unfolded protein response-induced ERdj3 secretion links ER stress to extracellular proteostasis.The EMBO journal · 2015Article
- Article
- Barcoding heat shock proteins to human diseases: looking beyond the heat shock response.Disease models & mechanisms · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is reaching epidemic proportions, yet a cure is not yet available. While the genetic causes of the rare familial inherited forms of AD are understood, the causes of the sporadic forms of the disease are not. Histopathologically, these two forms of AD are indistinguishable: they are characterized by amyloid-β (Aβ) peptide-containing amyloid plaques and tau-containing neurofibrillary tangles. In this review we compare AD to frontotemporal dementia (FTD), a subset of which is characterized by tau deposition in the absence of overt plaques. A host of transgenic animal AD models have been established through the expression of human proteins with pathogenic mutations previously identified in familial AD and FTD. Determining how these mutant proteins cause disease in vivo should contribute to an understanding of the causes of the more frequent sporadic forms. We discuss the insight transgenic animal models have provided into Aβ and tau toxicity, also with regards to mitochondrial function and the crucial role tau plays in mediating Aβ toxicity. We also discuss the role of miRNAs in mediating the toxic effects of the Aβ peptide.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.