APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia
Dementia is very common in the elderly and its incidence increases in an age-dependent fashion. Alzheimer''s disease and vascular cognitive decline are the most common cases of dementia in the elderly. Amyloid burden and increased levels of oxidative damage have been implicated to play sig...
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| Format: | Article |
| Language: | English |
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Pensoft Publishers
2015-09-01
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| Series: | BioDiscovery |
| Subjects: | |
| Online Access: | https://biodiscovery.pensoft.net/article/8969/download/pdf/ |
| _version_ | 1818158401683718144 |
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| author | Ashima Nayyar Lubomira Chakalova |
| author_facet | Ashima Nayyar Lubomira Chakalova |
| author_sort | Ashima Nayyar |
| collection | DOAJ |
| description | Dementia is very common in the elderly and its incidence increases in an age-dependent fashion. Alzheimer''s disease and vascular cognitive decline are the most common cases of dementia in the elderly. Amyloid burden and increased levels of oxidative damage have been implicated to play significant roles in the pathogenesis of late-onset dementia. In this paper we propose that there are three major genetic factors that may modulate the risk for dementia in later life: carriership of <em>APOE</em> variant alleles, carriership of mitochondrial DNA of haplogroups associated with ineffective oxygen utilisation (specifically, haplogroup H) and carriership of genetic polymorphisms conferring subtly deficient DNA repair. All three factors are quite common in the European populations. Each of these three factors may not have significant effect on the phenotype when taken separately, but when combined in the same genotype, the effects may be cumulative. Further studies are needed in order to elucidate the genotype-phenotype relationships and provide a reliable basis for assessment of the genetic risk for sporadic late-onset dementia. Lifestyle alterations and therapies targeted at decreasing the oxidative burden to aging cells and tissues may decrease the risk for neurological decline in later life. |
| first_indexed | 2024-12-11T15:29:30Z |
| format | Article |
| id | doaj.art-dc03fd0e93e04aff85e862d4e4420996 |
| institution | Directory Open Access Journal |
| issn | 2050-2966 |
| language | English |
| last_indexed | 2024-12-11T15:29:30Z |
| publishDate | 2015-09-01 |
| publisher | Pensoft Publishers |
| record_format | Article |
| series | BioDiscovery |
| spelling | doaj.art-dc03fd0e93e04aff85e862d4e44209962022-12-22T01:00:07ZengPensoft PublishersBioDiscovery2050-29662015-09-011711710.7750/BioDiscovery.2015.17.18969APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementiaAshima NayyarLubomira ChakalovaDementia is very common in the elderly and its incidence increases in an age-dependent fashion. Alzheimer''s disease and vascular cognitive decline are the most common cases of dementia in the elderly. Amyloid burden and increased levels of oxidative damage have been implicated to play significant roles in the pathogenesis of late-onset dementia. In this paper we propose that there are three major genetic factors that may modulate the risk for dementia in later life: carriership of <em>APOE</em> variant alleles, carriership of mitochondrial DNA of haplogroups associated with ineffective oxygen utilisation (specifically, haplogroup H) and carriership of genetic polymorphisms conferring subtly deficient DNA repair. All three factors are quite common in the European populations. Each of these three factors may not have significant effect on the phenotype when taken separately, but when combined in the same genotype, the effects may be cumulative. Further studies are needed in order to elucidate the genotype-phenotype relationships and provide a reliable basis for assessment of the genetic risk for sporadic late-onset dementia. Lifestyle alterations and therapies targeted at decreasing the oxidative burden to aging cells and tissues may decrease the risk for neurological decline in later life.https://biodiscovery.pensoft.net/article/8969/download/pdf/Late-onset diseasedementiaAPOEmitochondrial |
| spellingShingle | Ashima Nayyar Lubomira Chakalova APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia BioDiscovery Late-onset disease dementia APOE mitochondrial |
| title | APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia |
| title_full | APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia |
| title_fullStr | APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia |
| title_full_unstemmed | APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia |
| title_short | APOE4, oxidative stress and decreased repair capacity - a no-brainer. Faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late-onset dementia |
| title_sort | apoe4 oxidative stress and decreased repair capacity a no brainer faulty lipid metabolism and increased levels of oxidative damage may be risk factors in the pathogenesis of late onset dementia |
| topic | Late-onset disease dementia APOE mitochondrial |
| url | https://biodiscovery.pensoft.net/article/8969/download/pdf/ |
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