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Aneuploidy, chromosomal missegregation, and cell cycle reentry in Alzheimer's disease

100%

Zekanowski C. , Wojda U.

Acta Neurobiologiae Experimentalis

2009

tom 69

nr 2

232-253

Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Chromosome missegregation was proposed two decades ago to be responsible for neurodegeneration in AD patients. It was speculated that the aneuploidy is a result of aberrant cell cycle of neuronal progenitors during adult neurogenesis and/or of mature neurons. There is mounting evidence of increased rate of general aneuploidy and cell cycle reentry in the AD patients' brains, with area-specific pattern. In this review, we discuss the involvement of chromosome instability, genome damage and cell cycle impairment in AD pathology.

Editting and rearragement - two ways of transfomation of eucariotic genetic information

100%

Zekanowski C.

Biotechnologia

1994

nr 1

109-120

Mitochondrial DNA in pathogenesis of Alzheimer's and Parkinson's diseases

80%

Maruszak A. , Gaweda-Walerych K. , Soltyszewski I. , Zekanowski C.

Acta Neurobiologiae Experimentalis

2006

tom 66

nr 2

153-176

A critical role of mitochondrial dysfunction and oxidative damage has been implicated in etiopathology of many neurodegenerative disorders, as well as in normal aging. Alzheimer's and Parkinson's diseases are common devastating late-onset neurodegenerative disorders, associated with mitochondrial DNA variations, which are suggested to affect mitochondrial functions. This paper reviews the current knowledge on the inherited and somatic mtDNA variations in both conditions.

Genetic aspects of Alzheimer's disease

71%

Zekanowski C. , Religa D. , Graff C. , Filipek S. , Kuznicki J.

Acta Neurobiologiae Experimentalis

2004

tom 64

nr 1

19-31

Alzheimer's disease (AD) is a neurodegenerative disorder with a complex etiology and pathogenesis. Mutations in presenilin 1 gene (PSEN1), located on chromosome 14, more rarely in amyloid-beta protein precursor (APP) on chromosome 21, and presenilin 2 genes (PSEN2) on chromosome 1, underlie the pathogenesis of most cases of familial early onset of AD (EOAD). The genetics of late-onset AD (LOAD) have been more enigmatic and the only confirmed risk factor for LOAD remains the apolipoprotein E4 allele (ApoE4) on chromosome 19. In this review, we discuss the genetics of AD with a focus on the role of the APP and presenilins.