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Reducing HuD Levels Alleviates Alzheimer's Disease Pathology in 5xFAD Mice

1 year 5 months ago
Alzheimer's disease (AD) is the most common neurodegenerative pathology in older persons. The accumulation of amyloid β (Aβ) plaques is a major contributor to AD development. The RNA-binding protein HuD/ELAVL4 has been implicated in the formation of Aβ plaques, but its role in AD is unclear. Here, we report that ablation of HuD from CAMK2A^(+) neurons (HuDcKO) in the 5xFAD mouse model of AD results in a significant reduction of Aβ plaques and the alleviation of some AD-associated behaviors....
Eunbyul Ji

Mesenchymal stem cells and exosomes: A novel therapeutic approach for aging

1 year 5 months ago
Mesenchymal stem cells (MSCs), a vital component of the adult stem cell repertoire, are distinguished by their dual capacity for self-renewal and multilineage differentiation. The therapeutic effects of MSCs are primarily mediated through mechanisms such as homing, paracrine signaling, and cellular differentiation. Exosomes (Exos), a type of extracellular vesicles (EVs) secreted by MSCs via the paracrine pathway, play a pivotal role in conveying the biological functions of MSCs. Accumulating...
Dongfeng Lan

Elevated serum leucine levels are associated with cognitive impairment and reduced gray matter and cerebral volume across the Alzheimer's disease continuum

1 year 5 months ago
Leucine, a branched-chain amino acid (BCAA), exhibits paradoxical effects in Alzheimer's disease (AD), demonstrating both neuroprotective and neurotoxic roles. While prior studies have investigated leucine's systemic and metabolic impacts, its influence on brain structure remains unexplored. This study aimed to fill this critical gap by examining the relationship between serum leucine levels, brain volume metrics, and cognitive performance in individuals across the AD continuum. Serum leucine...
Hamide Nasiri

Cellular senescence promotes macrophage-to-myofibroblast transition in chronic ischemic renal disease

1 year 5 months ago
Cellular senescence participates in the pathophysiology of post-stenotic kidney damage, but how it regulates tissue remodeling is incompletely understood. Macrophage-myofibroblast transition (MMT) contributes to the development of tissue fibrosis. We hypothesized that cellular senescence contributes to MMT and renal fibrosis in mice with renal artery stenosis (RAS). INK-ATTAC mice expressing p16^(INK-4a) and green fluorescent protein in senescent cells were assigned to control or unilateral RAS,...
Yu Zhao