Results 31 to 40 of about 21,794 (134)
We present a pathology‐responsive, activity‐based prodrug strategy that tackles multiple hallmarks of Alzheimer's disease (AD). Rationally designed BE compounds convert under oxidative stress into redox‐active aminophenols, neutralizing ROS and redirecting both metal‐free and metal‐bound Aβ aggregation.
Jimin Lee +13 more
wiley +1 more source
Neuritic plaques increase in the intermediate stage of Alzheimer's neuropathological change. The intermediate stage of Alzheimer's disease was investigated by transcriptomics and immunohistochemistry. This revealed that inflammasome sensors NLRP1, NLRP3, and AIM2 oligomerize with ASC speck to form the inflammasome complex and initiate the downstream ...
Juan Pablo de Rivero Vaccari +10 more
wiley +1 more source
Proteostasis of organelles in aging and disease
Cells rely on regulated proteostasis mechanisms to keep their internal compartments functioning properly. When these mechanisms fail, damaged proteins accumulate, disrupting organelles, such as the nucleus, mitochondria, endoplasmic reticulum, Golgi, and lysosomes, as well as membraneless organelles, such as stress granules, processing bodies, the ...
Yara Nabawi +5 more
wiley +1 more source
Mitophagy in skeletal muscle: Impact of ageing, exercise and disuse
Abstract Skeletal muscle plays an important role in whole‐body health, quality of life and regulation of metabolism. The maintenance of a healthy mitochondrial pool is imperative for the preservation of skeletal muscle quality and is mediated through mitochondrial quality control consisting of mitochondrial turnover mediated by a balance between ...
Anastasiya Kuznyetsova, David A. Hood
wiley +1 more source
THE ROLES OF PRESENILIN-2 GENE IN THE APOPTOSIS OF MYOCARDIAL CELL [PDF]
Objectives Presenilin (PS) gene is a novel gene family of causative gene related with familial Alzheimer's disease. They have been detected not only in the brain, but also in some peripheral tissues including the heart. The main focus on the PS gene family was in central nervous system.
Hui Li, Yu Chen, Li Rao, Li Rao
openaire +1 more source
Abstract figure legend Mitochondria are highly dynamic organelles that continuously remodel their architecture through coordinated cycles of fusion and fission. This review examines the four key GTPases that orchestrate mitochondrial dynamics in mammals: MFN1, MFN2, OPA1, and DRP1.
Rémi Chaney +4 more
wiley +1 more source
SNPs in SH3RF3 decrease the age of onset of Alzheimer's disease (AD). Reduced SH3RF3 blunts human microglial JNK and NFkB signaling and downstream inflammatory cytokine production, which may partially explain how SH3RF3 SNPs protect against AD. ABSTRACT Understanding how high‐risk individuals are protected from Alzheimer's disease (AD) may illuminate ...
Ronak Patel +13 more
wiley +1 more source
Presenilin-2 modulation of ER-mitochondria interactions [PDF]
Presenilin (PS) mutations are the main cause of Familial Alzheimer's Disease (FAD) and have been demonstrated to cause an imbalance of intracellular Ca(2+) homeostasis. Though PS1 and 2 are generally considered to behave similarly in terms of their effects on Ca(2+) handling, we have recently described a novel function, which is unique to PS2, i.e ...
ZAMPESE, ENRICO +3 more
openaire +3 more sources
ABSTRACT Alzheimer's disease (AD) is a debilitating neurodegenerative condition characterized by progressive cognitive impairment, memory deterioration, and neuronal dysfunction. Its complex pathophysiology involves multiple interlinked processes, including amyloid‐β (Aβ) aggregation, tau hyperphosphorylation, oxidative stress, neuroinflammation ...
Amandeep Thakur +6 more
wiley +1 more source
ABSTRACT Aim The ryanodine receptor (RyR2) is an intracellular Ca2+ release channel which mediates numerous cellular functions across different tissues. Dysregulation of RyR2 channel activity leads to pathological Ca2+ release, which often underlies disrupted cellular signaling in disease states.
Michelle L. Munro +8 more
wiley +1 more source

