Amyloid, dementia and Alzheimer's disease
- PMID: 1623244
Amyloid, dementia and Alzheimer's disease
Abstract
Senile plaques (SP) and neurofibrillary tangles (NFT) are the major histopathological changes that occur in Alzheimer's disease (AD). How these two different types of lesions are related to each other and to the dementia of AD is unknown. Recent studies lead to paradoxical conclusions: NFT and neuronal alterations such as synapse loss are much more closely related to the symptoms of dementia than are SP. However, mutations in the beta-amyloid protein of SP have been found in some patients with familial AD, suggesting that an abnormality in amyloid causes the development of SP, NFT and AD dementia. Examination of transgenic animals that produce amyloid precursor protein (APP), or altered forms of APP, may lead to the development of an animal model of AD, and ultimately to answers that link amyloid production to neuronal alterations, and cognitive impairments.
Similar articles
-
The possible role of capillary cerebral amyloid angiopathy in Alzheimer lesion development: a regional comparison.Acta Neuropathol. 2006 Oct;112(4):417-27. doi: 10.1007/s00401-006-0099-z. Epub 2006 Jul 8. Acta Neuropathol. 2006. PMID: 16830133
-
Cerebral amyloid angiopathy and dementia.Panminerva Med. 2004 Dec;46(4):253-64. Panminerva Med. 2004. PMID: 15876981 Review.
-
[Involvement of beta-amyloid in the etiology of Alzheimer's disease].Brain Nerve. 2010 Jul;62(7):691-9. Brain Nerve. 2010. PMID: 20675873 Review. Japanese.
-
Non-tau based neuronal degeneration in Alzheimer's disease -- an immunocytochemical and quantitative study in the supragranular layers of the middle temporal neocortex.Brain Res. 2008 Jun 5;1213:152-65. doi: 10.1016/j.brainres.2008.03.043. Epub 2008 Apr 1. Brain Res. 2008. PMID: 18455153
-
Amyloid plaques, neurofibrillary tangles and neuronal loss in brains of transgenic mice overexpressing a C-terminal fragment of human amyloid precursor protein.Nature. 1991 Dec 12;354(6353):476-8. doi: 10.1038/354476a0. Nature. 1991. Retraction in: Nature. 1992 Mar 5;356(6364):23. doi: 10.1038/356023b0. Retraction in: Nature. 1992 Mar 19;356(6366):265. doi: 10.1038/356265a0. PMID: 1793460 Retracted.
Cited by
-
Active beta-amyloid immunization restores spatial learning in PDAPP mice displaying very low levels of beta-amyloid.J Neurosci. 2007 Mar 7;27(10):2654-62. doi: 10.1523/JNEUROSCI.3710-06.2007. J Neurosci. 2007. PMID: 17344403 Free PMC article.
-
Examining the diagnostic value of the mnemonic discrimination task for classification of cognitive status and amyloid-beta burden.Neuropsychologia. 2023 Dec 15;191:108727. doi: 10.1016/j.neuropsychologia.2023.108727. Epub 2023 Nov 7. Neuropsychologia. 2023. PMID: 37939874 Free PMC article.
-
Plaque-induced neurite abnormalities: implications for disruption of neural networks in Alzheimer's disease.Proc Natl Acad Sci U S A. 1999 Apr 27;96(9):5274-9. doi: 10.1073/pnas.96.9.5274. Proc Natl Acad Sci U S A. 1999. PMID: 10220456 Free PMC article.
-
Four-dimensional microglia response to anti-Aβ treatment in APP/PS1xCX3CR1/GFP mice.Intravital. 2013;2(2):e25693. doi: 10.4161/intv.25693. Epub 2013 Apr 1. Intravital. 2013. PMID: 28944103 Free PMC article.
-
Quantitative analysis of senile plaques in Alzheimer disease: observation of log-normal size distribution and molecular epidemiology of differences associated with apolipoprotein E genotype and trisomy 21 (Down syndrome).Proc Natl Acad Sci U S A. 1995 Apr 11;92(8):3586-90. doi: 10.1073/pnas.92.8.3586. Proc Natl Acad Sci U S A. 1995. PMID: 7724603 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical