Can mouse models mimic sporadic Alzheimer’s disease?
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia worldwide. As age is the main risk factor, > 97% of all AD cases are of sporadic origin, potentiated by various risk factors associated with life style and starting at an age > 60 years. O...
Main Authors: | , |
---|---|
Format: | Article |
Language: | English |
Published: |
Wolters Kluwer Medknow Publications
2020-01-01
|
Series: | Neural Regeneration Research |
Subjects: | |
Online Access: | http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=3;spage=401;epage=406;aulast=Foidl |
_version_ | 1818277513780002816 |
---|---|
author | Bettina M Foidl Christian Humpel |
author_facet | Bettina M Foidl Christian Humpel |
author_sort | Bettina M Foidl |
collection | DOAJ |
description | Alzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia worldwide. As age is the main risk factor, > 97% of all AD cases are of sporadic origin, potentiated by various risk factors associated with life style and starting at an age > 60 years. Only < 3% of AD cases are of genetic origin caused by mutations in the amyloid precursor protein or Presenilins 1 or 2, and symptoms already start at an age < 30 years. In order to study progression of AD, as well as therapeutic strategies, mouse models are state-of-the-art. So far many transgenic mouse models have been developed and used, with mutations in the APP or presenilin or combinations (3×Tg, 5×Tg). However, such transgenic mouse models more likely mimic the genetic form of AD and no information can be given how sporadic forms develop. Several risk genes, such as Apolipoprotein E4 and TREM-2 enhance the risk of sporadic AD, but also many risk factors associated with life style (e.g., diabetes, hypercholesterolemia, stress) may play a role. In this review we discuss the current situation regarding AD mouse models, and the problems to develop a sporadic mouse model of AD. |
first_indexed | 2024-12-12T23:02:44Z |
format | Article |
id | doaj.art-7bb7e9255d914509a65be6fa074efbfc |
institution | Directory Open Access Journal |
issn | 1673-5374 |
language | English |
last_indexed | 2024-12-12T23:02:44Z |
publishDate | 2020-01-01 |
publisher | Wolters Kluwer Medknow Publications |
record_format | Article |
series | Neural Regeneration Research |
spelling | doaj.art-7bb7e9255d914509a65be6fa074efbfc2022-12-22T00:08:47ZengWolters Kluwer Medknow PublicationsNeural Regeneration Research1673-53742020-01-0115340140610.4103/1673-5374.266046Can mouse models mimic sporadic Alzheimer’s disease?Bettina M FoidlChristian HumpelAlzheimer’s disease (AD) is a progressive neurodegenerative disorder and the most common form of dementia worldwide. As age is the main risk factor, > 97% of all AD cases are of sporadic origin, potentiated by various risk factors associated with life style and starting at an age > 60 years. Only < 3% of AD cases are of genetic origin caused by mutations in the amyloid precursor protein or Presenilins 1 or 2, and symptoms already start at an age < 30 years. In order to study progression of AD, as well as therapeutic strategies, mouse models are state-of-the-art. So far many transgenic mouse models have been developed and used, with mutations in the APP or presenilin or combinations (3×Tg, 5×Tg). However, such transgenic mouse models more likely mimic the genetic form of AD and no information can be given how sporadic forms develop. Several risk genes, such as Apolipoprotein E4 and TREM-2 enhance the risk of sporadic AD, but also many risk factors associated with life style (e.g., diabetes, hypercholesterolemia, stress) may play a role. In this review we discuss the current situation regarding AD mouse models, and the problems to develop a sporadic mouse model of AD.http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=3;spage=401;epage=406;aulast=FoidlAlzheimer’s disease; beta-amyloid; cerebral amyloid angiopathy; cognitive impairment; sporadic and genetic mouse models; tau; vascular risk factors |
spellingShingle | Bettina M Foidl Christian Humpel Can mouse models mimic sporadic Alzheimer’s disease? Neural Regeneration Research Alzheimer’s disease; beta-amyloid; cerebral amyloid angiopathy; cognitive impairment; sporadic and genetic mouse models; tau; vascular risk factors |
title | Can mouse models mimic sporadic Alzheimer’s disease? |
title_full | Can mouse models mimic sporadic Alzheimer’s disease? |
title_fullStr | Can mouse models mimic sporadic Alzheimer’s disease? |
title_full_unstemmed | Can mouse models mimic sporadic Alzheimer’s disease? |
title_short | Can mouse models mimic sporadic Alzheimer’s disease? |
title_sort | can mouse models mimic sporadic alzheimer s disease |
topic | Alzheimer’s disease; beta-amyloid; cerebral amyloid angiopathy; cognitive impairment; sporadic and genetic mouse models; tau; vascular risk factors |
url | http://www.nrronline.org/article.asp?issn=1673-5374;year=2020;volume=15;issue=3;spage=401;epage=406;aulast=Foidl |
work_keys_str_mv | AT bettinamfoidl canmousemodelsmimicsporadicalzheimersdisease AT christianhumpel canmousemodelsmimicsporadicalzheimersdisease |