Subgroups of Alzheimer's disease based on cerebrospinal fluid molecular markers

By K. Iqbal, M. Flory, S. Khatoon, Hilkka Soininen, T. Pirttila, M. Lehtovirta, I. Alafuzoff, Kaj Blennow, N. Andreasen, E. Vanmechelen and 1 more. 2005

166 citations recorded by the source corpus.

Subfields: Molecular Biology, Physiology, Psychiatry and Mental health

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

1. T. Wyss‐Coray
2. Ben Glocker
3. Ender Konukoglu

In Physiology

1. T. Wyss‐Coray
2. Ben Glocker
3. Ender Konukoglu

In Psychiatry and Mental health

1. Ben Glocker
2. Ender Konukoglu

Citations in the corpus

• Visual Feature Attribution Using Wasserstein GANs (2017, background): “In clinically oriented research, identifying subject-specific disease effects would be useful for stratification amongst the patient population and to help disentangling diseases such as AD [25] and Schizophrenia [48], that are believed to be composed of multiple sub-types rather than a single disea”
• Inflammation in Alzheimer disease: driving force, bystander or beneficial response? (2006, background): “Also, the role of immune and inflammatory processes may be more or less pronounced in different Alzheimer disease 'subtypes,' characterized by different levels of Aβ, tau and ubiquitin and the presence or absence of the apolipoprotein E ( APOE ) e 4 allel”
• Mechanisms of tau-induced neurodegeneration (2009, unknown): “, Ab1-42, total tau, and ubiquitin, five different subgroups of AD—ATEO, AELO, LEBALO, HARO, and ARTURO— have been identified [77].”
• Constructing Subject- and Disease-Specific Effect Maps: Application to Neurodegenerative Diseases (2016, background): “First, it would enable studying variations of conditions’ effects across the population to identify subgroups within the patients [18] and develop biomarkers of progression.”
• Reconstructing subject‐specific effect maps (2017, unknown): “In clinical and neuroscience research, subject-specific detections can be used for stratification and identification of subpopulations (Iqbal, 2005).”
• Two-year follow-up of amyloid deposition in patients with Alzheimer's disease. (2006, background): “One of the subjects showed a pathologically low CSF Ab 1-42 level (365 pmol/ml) but a low CSF tau value (75 pmol/ml) This illustrates the complexity in findings, as also recently described in CSF data by Iqbal et al. (2005).”