A Century of Alzheimer's Disease

By M. Goedert, M. Spillantini. Science, 2006

1,986 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/9dd6930ec19379110f95ed01d04363e92493dc73

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. K. Del Tredici
2. Yangling Mu
3. Fred H. Gage
4. H. Braak
5. T. Bird
6. Yigong Shi
7. Chang-En Yu
8. L. Bekris

In Molecular Biology

1. E. Mandelkow
2. K. Del Tredici
3. L. Ittner
4. M. Goedert
5. J. Götz
6. H. Braak
7. Fred H. Gage
8. T. Bird

In Physiology

1. K. Del Tredici
2. E. Mandelkow
3. M. Goedert
4. L. Ittner
5. J. Götz
6. H. Braak
7. T. Bird
8. Yigong Shi

Citations in the corpus

• NOA: a novel Network Ontology Analysis method (2011, background): “We identified the rewired protein interaction networks during the progression of Alzheimer’s disease (AD), which is a complex genetic disorder on nervous system affecting millions of elderly individuals worldwide (29).”
• Oxidative stress and the amyloid beta peptide in Alzheimer’s disease (2017, background): “One century later, this “unusual illness” named Alzheimer’s Disease (AD) has become the most widespread neurodegenerative disease whose etiology is still unknown[7].”
• Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases (2015, background): “4051 Goldman, S. M. (2014). Environmental toxins and Parkinson’s disease.”
• Oxidative Stress and the Pathogenesis of Alzheimer's Disease (2013, background): “Hyperphosphorylated tau protein is the major component of NFT, another hallmark of AD pathology that correlates with neurodegeneration and cognitive decline [6].”
• Alzheimer’s and Parkinson’s diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein (2015, positive): “Whereas abundant Ab plaques and cerebral vascular deposits are specific for AD, filamentous tau inclusions are also characteristic of other neurodegenerative diseases, including chronic traumatic encephalopathy (CTE), progressive supranuclear palsy (PSP), corticobasal degeneration (CBD), argyrophili”
• Animal models of Alzheimer's disease and frontotemporal dementia (2008, background): “, is unclear: in AD, tau is hyperphosphorylated, which reduces its association with microtubule”
• Expression of a noncoding RNA is elevated in Alzheimer's disease and drives rapid feed-forward regulation of β-secretase (2008, neutral): “dtd" [ ]> Sequential cleavage of amyloid precursor protein (APP) by BACE1, the β-site cleaving enzyme essential for Aβ 1–42 and amyloid-β 1–40 (Aβ 1–40) biosynthesi”
• EGCG redirects amyloidogenic polypeptides into unstructured, off-pathway oligomers (2008, background): “Here we examined the effect of EGCG on amyloid-β 1–42 (Aβ42) amyloidogenesis, which is implicated in the pathogenesis in AD [ 39 ].”
• Structural Polymorphism of 441-Residue Tau at Single Residue Resolution (2009, background): “Mutations in the tau gene cause tau aggregation and frontotemporal dementia with parkinsonism linked to Chromosome 17 [5,6].”
• Serine/threonine phosphatases: mechanism through structure. (2009, background): “Hyperphosphorylated Tau is thought to polymerize into neurofibrillary tangles in the brain and contributes to the onset of Alzheimer’s disease (Goedert and Spillantini, 2006).”
• EGCG remodels mature α-synuclein and amyloid-β fibrils and reduces cellular toxicity (2010, background): “Chafekar SM, Baas F, Scheper W (2008) Oligomer-specific Abeta toxicity in cell models is mediated by selective uptake.”
• Adult hippocampal neurogenesis and its role in Alzheimer's disease (2011, background): “Individuals with the disorder usually experience difficulties in learning, performance speed, recall accuracy and/or problem solving [1].”
• The pathological process underlying Alzheimer’s disease in individuals under thirty (2011, background): “Thus, the intraneuronal material seen here in young persons may be neither acutely toxic nor chronically benign: initially compatible with nerve cell survival, it may eventually result in cellular or axonal dysfunction [ 39 ] and, ultimately, even premature loss of involved neurons at certain sites.”