Abstract
Different factors interact to develop neurodegeneration in patients with dementia and other neurodegenerative disorders. Oxidative stress and the ε4 allele of apolipoprotein E (ApoE) are associated with significant alteration in lipid metabolism, in turn connected to a variety of neurodegenerative diseases and aging. Thus, a better understanding of the pathogenetic pathways associated with lipid dyshomeostasis may elucidate the causes of neurodegenerative processes. To address this issue, we evaluated the effects of antioxidant status and APOE genotype on neurodegeneration in patients with dementia of the Alzheimer type (AD), with vascular dementia (VaD), and in elderly healthy controls. Eighty-two AD, 42 VaD patients, and 26 healthy controls were recruited and underwent medial temporal lobe atrophy (MTA) assessment, white matter hyperintensities rating (WMH), serum total antioxidant status assaying (TAS), and APOE genotyping. A logistic regression algorithm applied to our data revealed that a 0.01 mmol/L decrease of TAS concentration increased the probability of MTA by 24% (p=0.038) and that carriers of the APOE ε4 allele showed higher WMH scores (p=0.018), confirming that small variations in antioxidant systems homeostasis are associated with relevant modifications of disease risk. Furthermore, in individuals with analogous TAS values, the presence of the ε4 allele increased the predicted probability of having MTA. These outcomes further sustain the interaction of oxidative stress and APOE genotype to neurodegeneration.
| Original language | English |
|---|---|
| Pages (from-to) | 51-56 |
| Number of pages | 6 |
| Journal | Rejuvenation Research |
| Volume | 16 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - Feb 1 2013 |
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ASJC Scopus subject areas
- Ageing
- Geriatrics and Gerontology
Cite this
Antioxidant status and APOE genotype as susceptibility factors for neurodegeneration in alzheimer's disease and vascular dementia. / Zito, Giancarlo; Polimanti, Renato; Panetta, Valentina; Ventriglia, Mariacarla; Salustri, Carlo; Siotto, Maria Cristina; Moffa, Filomena; Altamura, Claudia; Vernieri, Fabrizio; Lupoi, Domenico; Cassetta, Emanuele; Rossini, Paolo M.; Squitti, Rosanna.
In: Rejuvenation Research, Vol. 16, No. 1, 01.02.2013, p. 51-56.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Antioxidant status and APOE genotype as susceptibility factors for neurodegeneration in alzheimer's disease and vascular dementia
AU - Zito, Giancarlo
AU - Polimanti, Renato
AU - Panetta, Valentina
AU - Ventriglia, Mariacarla
AU - Salustri, Carlo
AU - Siotto, Maria Cristina
AU - Moffa, Filomena
AU - Altamura, Claudia
AU - Vernieri, Fabrizio
AU - Lupoi, Domenico
AU - Cassetta, Emanuele
AU - Rossini, Paolo M.
AU - Squitti, Rosanna
PY - 2013/2/1
Y1 - 2013/2/1
N2 - Different factors interact to develop neurodegeneration in patients with dementia and other neurodegenerative disorders. Oxidative stress and the ε4 allele of apolipoprotein E (ApoE) are associated with significant alteration in lipid metabolism, in turn connected to a variety of neurodegenerative diseases and aging. Thus, a better understanding of the pathogenetic pathways associated with lipid dyshomeostasis may elucidate the causes of neurodegenerative processes. To address this issue, we evaluated the effects of antioxidant status and APOE genotype on neurodegeneration in patients with dementia of the Alzheimer type (AD), with vascular dementia (VaD), and in elderly healthy controls. Eighty-two AD, 42 VaD patients, and 26 healthy controls were recruited and underwent medial temporal lobe atrophy (MTA) assessment, white matter hyperintensities rating (WMH), serum total antioxidant status assaying (TAS), and APOE genotyping. A logistic regression algorithm applied to our data revealed that a 0.01 mmol/L decrease of TAS concentration increased the probability of MTA by 24% (p=0.038) and that carriers of the APOE ε4 allele showed higher WMH scores (p=0.018), confirming that small variations in antioxidant systems homeostasis are associated with relevant modifications of disease risk. Furthermore, in individuals with analogous TAS values, the presence of the ε4 allele increased the predicted probability of having MTA. These outcomes further sustain the interaction of oxidative stress and APOE genotype to neurodegeneration.
AB - Different factors interact to develop neurodegeneration in patients with dementia and other neurodegenerative disorders. Oxidative stress and the ε4 allele of apolipoprotein E (ApoE) are associated with significant alteration in lipid metabolism, in turn connected to a variety of neurodegenerative diseases and aging. Thus, a better understanding of the pathogenetic pathways associated with lipid dyshomeostasis may elucidate the causes of neurodegenerative processes. To address this issue, we evaluated the effects of antioxidant status and APOE genotype on neurodegeneration in patients with dementia of the Alzheimer type (AD), with vascular dementia (VaD), and in elderly healthy controls. Eighty-two AD, 42 VaD patients, and 26 healthy controls were recruited and underwent medial temporal lobe atrophy (MTA) assessment, white matter hyperintensities rating (WMH), serum total antioxidant status assaying (TAS), and APOE genotyping. A logistic regression algorithm applied to our data revealed that a 0.01 mmol/L decrease of TAS concentration increased the probability of MTA by 24% (p=0.038) and that carriers of the APOE ε4 allele showed higher WMH scores (p=0.018), confirming that small variations in antioxidant systems homeostasis are associated with relevant modifications of disease risk. Furthermore, in individuals with analogous TAS values, the presence of the ε4 allele increased the predicted probability of having MTA. These outcomes further sustain the interaction of oxidative stress and APOE genotype to neurodegeneration.
UR - http://www.scopus.com/inward/record.url?scp=84874279735&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84874279735&partnerID=8YFLogxK
U2 - 10.1089/rej.2012.1383
DO - 10.1089/rej.2012.1383
M3 - Article
C2 - 23216585
AN - SCOPUS:84874279735
VL - 16
SP - 51
EP - 56
JO - Rejuvenation Research
JF - Rejuvenation Research
SN - 1549-1684
IS - 1
ER -