Genomes and Genes
Affiliation: Frankfurt am Main
- Age-dependent association between butyrylcholinesterase K-variant and Alzheimer disease-related neuropathology in human brainsEstifanos Ghebremedhin
Department of Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, 60590 Frankfurt, Germany
Neurosci Lett 320:25-8. 2002..036 for NFTs, and P=0.045 for A beta-deposits) at ages > or = 70 years but not 50-69 years. Furthermore, no interaction was apparent between BCHE-K and ApoE...
- Argyrophilic grain disease is associated with apolipoprotein E epsilon 2 alleleE Ghebremedhin
Department of Anatomy, J W Goethe University, Frankfurt Main, Germany
Acta Neuropathol 96:222-4. 1998..0002). The association between AGD and epsilon2 allele of ApoE suggests that AGD can be distinguished from other neurodegenerative disorders not only neuropathologically, but also genetically...
- Gender and age modify the association between APOE and AD-related neuropathologyE Ghebremedhin
Department of Clinical Neuroanatomy, J W Goethe University, Frankfurt, Germany
Neurology 56:1696-701. 2001..To assess the impact of apolipoprotein E (APOE) polymorphism on AD-related neurofibrillary tangle (NFT) formation and senile plaques (SP)...
- Genetic association of argyrophilic grain disease with polymorphisms in alpha-2 macroglobulin and low-density lipoprotein receptor-related protein genesE Ghebremedhin
Department of Clinical Neuroanatomy, J W Goethe University, Frankfurt Main, Germany
Neuropathol Appl Neurobiol 28:308-13. 2002..9% vs. 13.2%, P=0.93). This association, however, is only apparent in the presence of the LRP CC genotype. In conclusion, the present study shows that AGD is associated with the LRP, A2M and ApoE genes...
- Homozygosity for the K variant of BCHE gene increases the risk for development of neurofibrillary pathology but not amyloid deposits at young agesEstifanos Ghebremedhin
Institute of Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Acta Neuropathol 114:359-63. 2007..These findings suggest that homozygosity, but not heterozygosity, for BCHE-K is a potential risk factor for the development of NFT pathology in young individuals implicating BCHE-K in the pathogenesis of early AD...
- Relationship of apolipoprotein E and age at onset to Parkinson disease neuropathologyEstifanos Ghebremedhin
Institute for Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, D 60590 Frankfurt Main, Germany
J Neuropathol Exp Neurol 65:116-23. 2006..001). In conclusion, our findings suggest that APOE may express its effect on the risk of PD by modifying the occurrence of PD pathology, but age of PD onset seems to be the principal determinant of the progression rate of PD pathology...
- Two types of sporadic cerebral amyloid angiopathyDietmar Rudolf Thal
Department of Clinical Neuroanatomy, J W Goethe University, Frankfurt am Main, Germany
J Neuropathol Exp Neurol 61:282-93. 2002..CAA-Type 2 is not associated with the epsilon4 allele as a risk factor but shows a higher epsilon2 allele frequency than CAA-Type 1 cases and controls in our sample...
- Inverse relationship between cerebrovascular lesions and severity of lewy body pathology in patients with lewy body diseasesEstifanos Ghebremedhin
Institute for Clinical Neuroanatomy, J W Goethe University, Frankfurt Main, Germany
J Neuropathol Exp Neurol 69:442-8. 2010..05 each). In conclusion, DLB and PD patients with advanced LB pathology were less likely to show severe cerebrovascular disease or history of stroke...
- High prevalence of thorn-shaped astrocytes in the aged human medial temporal lobeChristian Schultz
Institute for Clinical Neuroanatomy, Johann Wolfgang Goethe University, 60590 Frankfurt Main, Germany
Neurobiol Aging 25:397-405. 2004..In summary, this study suggests that TSA is a distinct form of glial tau pathology that occurs with a high frequency in elderly individuals...
- Coincident enrichment of phosphorylated IkappaBalpha, activated IKK, and phosphorylated p65 in the axon initial segment of neuronsChristian Schultz
Institute for Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, D 60590 Frankfurt, Germany
Mol Cell Neurosci 33:68-80. 2006..These data provide the first evidence for a compartmentalized clustering of NF-kappaB pathway components in the AIS and implicate this neuronal compartment in the activation of NF-kappaB...
- Stages in the development of Parkinson's disease-related pathologyHeiko Braak
Institute for Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, 60590 Frankfurt Main, Germany
Cell Tissue Res 318:121-34. 2004..At this point, most individuals probably cross the threshold to the symptomatic phase of the illness. In the end-stages 5-6, the process enters the mature neocortex, and the disease manifests itself in all of its clinical dimensions...
- Diminished tyrosine hydroxylase immunoreactivity in the cardiac conduction system and myocardium in Parkinson's disease: an anatomical studyEstifanos Ghebremedhin
Institute of Clinical Neuroanatomy, Goethe University Frankfurt, 60590, Frankfurt am Main, Germany
Acta Neuropathol 118:777-84. 2009....
- Vessel ultrastructure in APP23 transgenic mice after passive anti-Abeta immunotherapy and subsequent intracerebral hemorrhageGuido J Burbach
Institute of Clinical Neuroanatomy, J W Goethe University, Theodor Stern Kai 7, D 60590 Frankfurt, Germany
Neurobiol Aging 28:202-12. 2007..Minor structural alterations of the vessel wall, however, cannot be excluded due to the sample size of our study and the high complexity of the three-dimensional vessel wall ultrastructure...
- Spinocerebellar ataxia type 3 (SCA3): thalamic neurodegeneration occurs independently from thalamic ataxin-3 immunopositive neuronal intranuclear inclusionsUdo Rüb
Institute for Clinical Neuroanatomy, Johann Wolfgang Goethe Univeristy, Frankfurt Main, Germany
Brain Pathol 16:218-27. 2006..This lack of correlation may suggest that ataxin-3 immunopositive NI are not immediately decisive for the fate of affected nerve cells but rather represent unspecific and pathognomonic morphological markers of SCA3...
- Cerebral amyloid angiopathy and cortical microinfarcts as putative substrates of vascular dementiaMattias Haglund
Division of Neuropathology, Department of Pathology and Cytology, Lund University Hospital, Sweden
Int J Geriatr Psychiatry 21:681-7. 2006..Therefore, we investigated the presence and characteristics of CAA in brains of VaD cases...
- The biphasic relationship between regional brain senile plaque and neurofibrillary tangle distributions: modification by age, sex, and APOE polymorphismElizabeth H Corder
Duke University, Center for Demographic Studies, Durham, NC 27708 0408, USA
Ann N Y Acad Sci 1019:24-8. 2004..The gender gap in SPs at early NFT stages was large and specific to women who carried the APOE4 allele (P <.001) and in addition to the acceleration in NFT stage also found for APOE4+ women...
- Increased brain beta-amyloid load, phosphorylated tau, and risk of Alzheimer disease associated with an intronic CYP46 polymorphismAndreas Papassotiropoulos
Division of Pychiatry Research, University of Zurich, Switzerland
Arch Neurol 60:29-35. 2003..CYP46, the gene encoding cholesterol 24-hydroxylase, plays a key role in the hydroxylation of cholesterol and thereby mediates its removal from brain...
- Cerebral small vessel disease-induced apolipoprotein E leakage is associated with Alzheimer disease and the accumulation of amyloid beta-protein in perivascular astrocytesSabrina Utter
Department of Neuropathology, University of Bonn, Bonn, Germany
J Neuropathol Exp Neurol 67:842-56. 2008..It is therefore tempting to speculate that apoE represents a pathogenetic link between SVD and AD...
- Molecular evolution and genetics of the Saitohin gene and tau haplotype in Alzheimer's disease and argyrophilic grain diseaseChris Conrad
Department of Pathology, Albert Einstein College of Medicine, Bronx, New York, USA
J Neurochem 89:179-88. 2004..More detailed studies confirm the H2 haplotype to be the ancestral tau gene. This situation is reminiscent of the evolution of the apolipoprotein (ApoE) gene, another locus that is potentially important for the risk of development of AD...
- Apolipoprotein E co-localizes with newly formed amyloid beta-protein (Abeta) deposits lacking immunoreactivity against N-terminal epitopes of Abeta in a genotype-dependent mannerDietmar Rudolf Thal
Department of Neuropathology, University of Bonn, Sigmund Freud Str 25, 53127 Bonn, Germany
Acta Neuropathol 110:459-71. 2005..Moreover, apoE-positive newly formed plaques were seen more frequently in APOE epsilon4/4 cases than in non-APOE epsilon4/4 individuals, thereby underlining the potentially crucial role of apoE for the development of Abeta deposits...
- Vascular pathology in Alzheimer disease: correlation of cerebral amyloid angiopathy and arteriosclerosis/lipohyalinosis with cognitive declineDietmar Rudolf Thal
Department of Neuropathology, University of Bonn Medical Center, Bonn, Germany
J Neuropathol Exp Neurol 62:1287-301. 2003..A combination of both CAA and AS/LH may, therefore, contribute to neurodegeneration in AD. These data also suggest that small vessel disease due to arteriosclerosis and fibrolipohyalinosis is a potential target for the treatment of AD...
- Cerebral amyloid angiopathy and its relationship to Alzheimer's diseaseDietmar Rudolf Thal
Laboratory of Neuropathology, Institute of Pathology, University of Ulm, Albert Einstein Allee 7, 89081 Ulm, Germany
Acta Neuropathol 115:599-609. 2008..Thus, blood flow alterations with subsequent hypoperfusion induced by CAA-related capillary occlusion presumably point to a second mechanism in which A beta adversely affects the brain in AD in addition to its direct neurotoxic effects...