The pathological process underlying Alzheimer’s disease in individuals under thirty
By H. Braak, K. Del Tredici. Acta Neuropathologica, 2011
805 citations recorded by the source corpus.
Subfields: Molecular Biology, Neurology, Physiology
View Paper: https://www.semanticscholar.org/paper/85a0d8744e2c50e4342e7072e97ffbe60166e38d
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- D. Holtzman
- K. Del Tredici
- Lary C. Walker
- Mathias Jucker
- H. Braak
- D. Thal
- E. Ghebremedhin
- John Q. Trojanowski
In Neurology
- Dennis W. Dickson
- D. Holtzman
- K. Del Tredici
- H. Braak
- John Q. Trojanowski
- Mathias Jucker
- Lary C. Walker
- E. Ghebremedhin
In Physiology
- D. Holtzman
- Dennis W. Dickson
- Clifford R. Jack Jr.
- Kaj Blennow
- John C. Morris
- Reisa A. Sperling
- John Q. Trojanowski
- K. Del Tredici
Citations in the corpus
- Alzheimer’s Disease: The Challenge of the Second Century (2011, background): “There is also a typical progression of tau pathology within specific brain networks in normal aging and in AD, starting first in areas such as the brainstem and transentorhinal region (23, 42) and then spreading throughout the limbic system and other regions of the neocortex.”
- Using mice to model Alzheimer's dementia: an overview of the clinical disease and the preclinical behavioral changes in 10 mouse models (2014, background): “In the earliest stages of AD (Braak stage I-II), NFTs are restricted to the entorhinal cortex (Braak and Del Tredici, 2011; Braak et al., 2011).”
- The Alzheimer’s Disease Neuroimaging Initiative: A review of papers published since its inception (2011, positive): “However, although ADNI and other biomarker data support this sequence of events, by direct examination of postmortem human brains, Braak andDel Tredici have shown that tau pathology in themedial temporal limbic isocortex precedes the development of Ab deposits with advancing age in the human brain [”
- Alzheimer’s and Parkinson’s diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein (2015, neutral): “In the human brain, neurofibrillary lesions appear to spread along neural pathways from one brain region to another (62, 73).”
- Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 Years (2011, methodology): “A set of 2 tissue blocks was excised, embedded in polyethylene glycol (PEG 1000; Merck, Darmstadt, Germany), and sectioned at 100 Km, as previously described (4, 8, 20).”
- Primary age-related tauopathy (PART): a common pathology associated with human aging (2014, background): “The rationale for including extracortical tau pathology in PART is that the pathologies commonly coexist and that brain-stem NFTs, if they represent the same process, appear to occur even earlier in human aging [30–32 , 53 ].”
- Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012, background): “At 40 years, all individuals studied by Braak and Del Tredici (39) and Braak et al (44) exhibited at least initial neurofibrillary pathology in the brain-stem (Fig.”
- Pathogenic Protein Seeding in Alzheimer’s Disease and Other Neurodegenerative Disorders (2011, background): “In the brain, neurofibrillary tangles (B) occur first in the locus coeruleus and transentorhinal area and then spread to the amygdala and interconnected neocortical brain regions.(8,24) The relatively stereotyped patterns of expansion suggest the involvement of neuronal transport mechanisms in the s”
- National Institute on Aging–Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease (2012, neutral): “NFTs commonly are observed in limbic regions early in the disease but, depending on disease stage, also involve other brain regions, including association cortex, some subcortical nuclei, and even some brainstem regions [28], where their formation may precede that in limbic structures [29].”