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| Titel: |
DNA Damage does not Correlate with Amyloid-ß-Plaques and Neurofibrillary Tangles in Familial Alzheimer's Disease Presenilin-1 [E280A] Mutation |
| Auteur: |
C. Velez-Pardo F. Lopera M. Jimenez Del Rio |
| Verschenen in: |
Journal of Alzheimer's disease |
| Paginering: | Jaargang 2 (2001) nr. 1 pagina's 47-57 |
| Jaar: |
2001-04-01 |
| Inhoud: |
Recent studies have shown that the missense mutation in presenilin-1 [E280A] increases deposition of amyloid-â (Aâ[1-42/43]) producing severe cerebellar pathology. Although Aâ has been involved as a neurotoxic peptide, its role in neuronal loss in PS-1 [E280A] patients has not yet been established. This study investigated terminal fluorescein 12-dUTP nick-end labeling (TUNEL)-positive cells (neuron, glia and microglial cells) and thioflavine S-stained Aâ-plaques and neurofibrillary tangles in the frontal, parietal, temporal, occipital, hippocampus and cerebellum cortices of 3 normal aging and 8 familial Alzheimer's disease patients with the presenilin-1 [E280A] mutation. Using these approaches, we found no obvious correlation between DNA fragmentation and the severity of amyloid-â deposition (Aâ) and neurofibrillary tangle (NFT) formation. Indeed, we only observed 10 out of 48 FAD brain sections displaying TUNEL (+) labeling, and none with the classical apoptotic morphology. These results may indicate that DNA fragmentation is not a generalized phenomenon in early-onset FAD PS1 [E280A] patients or that neuronal cells are dying by a different mechanism of cell death. Taking together these findings suggest that Aâ and NFTs are not per se a causative factor to damage neuronal cells but their damage could be more related with individual neuronal vulnerability and brain aging |
| Uitgever: |
IOS Press |
| Bronbestand: |
Elektronische Wetenschappelijke Tijdschriften |
Details van artikel 5 van 7 gevonden artikelen
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