GR Frost, YM Li - Open biology, 2017 - royalsocietypublishing.org
Alzheimer's disease (AD) is marked by the presence of extracellular amyloid beta (Aβ) plaques, intracellular neurofibrillary tangles (NFTs) and gliosis, activated glial cells, in the …
L Sun, R Zhou, G Yang, Y Shi - Proceedings of the National …, 2017 - National Acad Sciences
A hallmark of Alzheimer's disease (AD) is the aggregation of β-amyloid peptides (Aβ) into amyloid plaques in patient brain. Cleavage of amyloid precursor protein (APP) by the …
RJ Kelleher III, J Shen - Proceedings of the National …, 2017 - National Acad Sciences
Mutations in the PSEN1 gene, encoding presenilin-1 (PS1), are the most common cause of familial Alzheimer's disease (FAD). PS1 functions as the catalytic subunit of γ-secretase, an …
J Bagaria, E Bagyinszky, SSA An - International Journal of Molecular …, 2022 - mdpi.com
Presenilin-1 (PSEN1) has been verified as an important causative factor for early onset Alzheimer's disease (EOAD). PSEN1 is a part of γ-secretase, and in addition to amyloid …
Alzheimer's disease (AD) is the disease of lost memories. Synaptic loss is a major reason for memory defects in AD. Signaling pathways involved in memory loss in AD are under intense …
MH Dai, H Zheng, LD Zeng, Y Zhang - Oncotarget, 2018 - ncbi.nlm.nih.gov
Alzheimer's disease (AD) is a progressive neurodegenerative disorder that accounts for the most cases of dementia, which is characterized by the deposition of dense plaques of …
MA Greenough, DJR Lane, R Balez… - Cell Death & …, 2022 - nature.com
Mutations in presenilin 1 and 2 (PS1 and PS2) cause autosomal dominant familial Alzheimer's disease (FAD). Ferroptosis has been implicated as a mechanism of …
The elimination of abnormal and dysfunctional cellular constituents is an essential prerequisite for nerve cells to maintain their homeostasis and proper function. This is mainly …
Recently it was proposed that the familial Alzheimer's disease (FAD) causing presenilin (PSEN) mutations PSEN1-L435F and PSEN1-C410Y do not support the generation of Aβ …