Molecular Pathology of Alzheimer's Disease

By R. Castellani, George Perry. 2013

1,086 citations recorded by the source corpus.

Subfields: Computational Theory and Mathematics, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/6727fd147f3d6acb58a291646941349e8ddc4a2f

How researchers see this paper

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

In Computational Theory and Mathematics

1. D. Selkoe
2. D. Walsh
3. K. Ashe
4. G. Shankar
5. John Hardy
6. Louise C. Serpell
7. R. Swerdlow
8. P. Reddy

In Molecular Biology

1. D. Selkoe
2. S. Bensinger
3. G. Shankar
4. John Hardy
5. Louise C. Serpell
6. D. Walsh
7. C. Zhong
8. P. Tontonoz

In Physiology

1. D. Selkoe
2. G. Shankar
3. D. Walsh
4. John Hardy
5. K. Ashe
6. Louise C. Serpell
7. C. Zhong
8. P. Tontonoz

Citations in the corpus

• Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease (2018, background): “…(also known as the amyloid cascade hypothesis, the Aβ hypothesis, etc.) has been the mainstream explanation for the pathogenesis of AD for over 25 years (Hardy and Allsop, 1991; Selkoe, 1991; Hardy and Higgins, 1992; Hardy and Selkoe, 2002), and may be briefly summarized as follows (Figure 1).”
• Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. (2008, background): “A wealth of data from many laboratories now supports the once controversial hypothesis that the accumulation and aggregation of Aβ initiates a complex cascade of molecular and cellular changes that gradually leads to the clinical features of MCI-amnestic type and then frank Alzheimer’s disease (Hard”
• Integration of metabolism and inflammation by lipid-activated nuclear receptors (2008, background): “Alzheimer's disease is an age-dependent neurodegenerative disorder that results in progressive cognitive deficit”
• GABAergic Interneuron Dysfunction Impairs Hippocampal Neurogenesis in Adult Apolipoprotein E4 Knock-in Mice (2009, background): “The hippocampus is one of the first regions of the brain damaged in AD, and memory deficits and disorientation are among the early symptoms (Selkoe, 1991; Tanzi and Bertram, 2001).”
• Memantine treatment in patients with moderate to severe Alzheimer disease already receiving donepezil: a randomized controlled trial. (2004, background): “Pathological features of AD include intraneuronal neurofibrillary tangles containing abnormally phosphorylated tau protein, extracellular amyloid plaques containing the peptide amyloid, neuronal cell death, and anatomic as well as functional impairment of neurotransmitter systems.(1,2) Alzheimer dis”
• Deciphering the molecular basis of memory failure in Alzheimer's disease. (2004, background): “, Selkoe, D.J., and Wolfe, M.S. P.M., Teplow, D.B., and Selkoe, D.J. (1999). Protofibrillar intermedi(2000). Transition-state analogue inhibitors of -secretase bind di- ates of amyloid -protein induce acute electrophysiological changes rectly to presenilin-1.”
• Natural oligomers of the amyloid-β protein specifically disrupt cognitive function (2005, background): “β-amyloid(1-40) effects on behavior and memory.”
• The amyloid hypothesis of Alzheimer's disease at 25 years (2016, background): “Nat Genet 45: 1452 – 1458 Lemere CA, Blustzjan JK, Yamaguchi H, Wisniewski T, Saido TC, Selkoe DJ (1996a) Sequence of deposition of heterogeneous amyloid b-peptides and Apo E in Down syndrome: implications for initial events in amyloid plaque formation.”
• Random forest-based similarity measures for multi-modal classification of Alzheimer's disease (2013, neutral): “According to the amyloid cascade hypothesis, the disease process begins with the formation of insoluble β-amyloid (Aβ) plaques, whose presence triggers the hyperphosphorylation of tau protein, ultimately leading to cell death (Selkoe, 1991).”
• Alzheimer's amyloid fibrils: structure and assembly. (2000, background): “Alzheimer's disease is characterised by the deposition of insoluble amyloid ¢brils as amyloid plaques in the neuropil as well as the accumulation of neuro¢brillary tangles in cell bodies of neurones [1].”
• Decoding Alzheimer's disease from perturbed cerebral glucose metabolism: implications for diagnostic and therapeutic strategies. (2013, background): “There have been a huge number of studies on AD pathogeneses, including b-amyloid (Ab) hypothesis (Hardy and Selkoe, 2002; Hardy and Higgins, 1992; Selkoe, 1991) and tau hyperphosphorylation hypothesis (Grundke-Iqbal et al.”