2017
DOI: 10.1186/s12883-017-0942-y
|View full text |Cite
|
Sign up to set email alerts
|

Can brain impermeable BACE1 inhibitors serve as anti-CAA medicine?

Abstract: BackgroundCerebral amyloid angiopathy (CAA) is characterized by the deposition of ß-amyloid peptides (Aß) in and surrounding the wall of microvasculature in the central nervous system, together with parenchymal amyloid plaques collectively referred to as cerebral amyloidosis, which occurs in the brain commonly among the elderly and more frequently in patients with Alzheimer’s disease (AD). CAA is associated with vascular injury and may cause devastating neurological outcomes. No therapeutic approach is availab… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1

Citation Types

0
2
0

Year Published

2018
2018
2021
2021

Publication Types

Select...
5

Relationship

1
4

Authors

Journals

citations
Cited by 6 publications
(2 citation statements)
references
References 162 publications
(163 reference statements)
0
2
0
Order By: Relevance
“…The triple-transgenic mouse model of AD (3×Tg-AD) also harbors a mutant human tau (P301L) gene associated with frontotemporal dementia [ 7 ] and develops both plaque- and tangle-like pathologies in the brain [ 8 ]. Transgenic AD models are widely used in exploratory studies and have provided insights into the biological, pathogenic, and behavioral/cognitive underpinnings of this disease [ 2 , 3 , 9 , 10 ]. These animal models have also served as a prime system for the development and evaluation of various AD therapeutic approaches [ 1 , 11 , 12 ].…”
Section: Introductionmentioning
confidence: 99%
“…The triple-transgenic mouse model of AD (3×Tg-AD) also harbors a mutant human tau (P301L) gene associated with frontotemporal dementia [ 7 ] and develops both plaque- and tangle-like pathologies in the brain [ 8 ]. Transgenic AD models are widely used in exploratory studies and have provided insights into the biological, pathogenic, and behavioral/cognitive underpinnings of this disease [ 2 , 3 , 9 , 10 ]. These animal models have also served as a prime system for the development and evaluation of various AD therapeutic approaches [ 1 , 11 , 12 ].…”
Section: Introductionmentioning
confidence: 99%
“…Finally, the increase in Aβ accumulation (hit two) accelerates neuronal dysfunction, NFT formation, neurodegeneration, and dementia [29] (Figure 3, step 4). [117]. [118] Verubecestat/NCT01739348 ¥ III [119] Umibecestat/NCT01097096 ¥ III [120] LY2886721/NCT01561430 ¥ III [121] (b) Gamma-secretase inhibitors and modulators Semagacestat/NCT00594568 ¥ III Effect on NVU cells.…”
Section: The Two-hit Vascular Hypothesis and Dysfunction Of The Nvumentioning
confidence: 99%