K Schindowski
Overview
Explore the profile of K Schindowski including associated specialties, affiliations and a list of published articles.
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13
Citations
370
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Recent Articles
1.
Belarbi K, Burnouf S, Fernandez-Gomez F, Desmercieres J, Troquier L, Brouillette J, et al.
Curr Alzheimer Res
. 2011 May;
8(6):633-8.
PMID: 21605043
Alzheimer's disease (AD) is a neurodegenerative disorder histologically defined by the cerebral accumulation of amyloid deposits and neurofibrillary tangles composed of hyperphosphorylated tau proteins. Loss of basal forebrain cholinergic neurons...
2.
Schindowski K, Belarbi K, Bretteville A, Ando K, Buee L
Genes Brain Behav
. 2008 Feb;
7 Suppl 1:92-100.
PMID: 18184373
The aim of the present study was to investigate the relation between neurogenesis, cell cycle reactivation and neuronal death during tau pathology in a novel tau transgenic mouse line THY-Tau22...
3.
Schindowski K, Belarbi K, Buee L
Genes Brain Behav
. 2008 Feb;
7 Suppl 1:43-56.
PMID: 18184369
Neurotrophic factors (NTF) are small, versatile proteins that maintain survival and function to specific neuronal populations. In general, the axonal transport of NTF is important as not all of them...
4.
Leuner K, Pantel J, Frey C, Schindowski K, Schulz K, Wegat T, et al.
J Neural Transm Suppl
. 2007 Nov;
(72):207-15.
PMID: 17982897
Alzheimer's disease (AD) is the most common progressive neurodegenerative disease. Today, AD affects millions of people worldwide and the number of AD cases will increase with increased life expectancy. The...
5.
Krause S, Schindowski K, Zechel S, von Bohlen Und Halbach O
J Neurosci Res
. 2007 Sep;
86(2):411-21.
PMID: 17828769
The neurotrophin brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) and their cognate receptors, trkB and trkC, have a variety of physiological brain functions, ranging from cell survival to mechanisms involved...
6.
Schindowski K, Peters J, Gorriz C, Schramm U, Weinandi T, Leutner S, et al.
Pharmacopsychiatry
. 2006 Nov;
39(6):220-8.
PMID: 17124644
Background: Immunotherapy appears to be a potent treatment against Alzheimer's disease (AD), but the mechanisms underlying neural-immune interaction are still not known. Methods: Here, we determined cell death and distribution...
7.
Leutner S, Schindowski K, Frolich L, Maurer K, Kratzsch T, Eckert A, et al.
Pharmacopsychiatry
. 2005 Dec;
38(6):312-5.
PMID: 16342003
Introduction: Reactive oxygen species (ROS) have been implicated in neurodegeneration and seem to be involved in the physiology and pathophysiology of several diseases, including normal aging and Alzheimer's disease (AD)....
8.
Eckert A, Keil U, Kressmann S, Schindowski K, Leutner S, Leutz S, et al.
Pharmacopsychiatry
. 2003 Sep;
36 Suppl 1:S15-23.
PMID: 13130384
As major sources of reactive oxygen species (ROS), mitochondrial structures are exposed to high concentrations of ROS and may therefore be particularly susceptible to oxidative damage. Mitochondrial damage could play...
9.
Schindowski K, Leutner S, Kressmann S, Eckert A, Muller W
J Neural Transm (Vienna)
. 2001 Nov;
108(8-9):969-78.
PMID: 11716149
Enhanced apoptosis and elevated levels of reactive oxygen species (ROS) play a major role in aging. In addition, several neurodegenerative diseases are associated with increased oxidative stress and apoptosis in...
10.
Eckert A, Schindowski K, Leutner S, Luckhaus C, Touchet N, Czech C, et al.
Neurobiol Dis
. 2001 Apr;
8(2):331-42.
PMID: 11300728
Many cases of early-onset inherited Alzheimer's disease (AD) are caused by mutations in the presenilin-1 (PS1) gene. Expression of PS1 mutations in cell culture systems and in primary neurons from...