Increased fragility of neuronal membranes with aging.

Neuronal and microglial cathepsins in aging and age-related diseases.

It has been long believed that cathepsins compensate for each other because of their overlapping substrate specificities. However, there is increasing evidence that disturbance of the normal balance of their enzymatic activities is the first insult in brain aging and age-related diseases. The imbalance of cathepsins may further cause age-related neuropathological changes such as accumulation of...

Aging and fragility of bone.

Biophysical and Biochemical Markers of Red Blood Cell Fragility.

BACKGROUND Red blood cells (RBCs) undergo a natural aging process occurring in the blood circulation throughout the RBC lifespan or during routine cold storage in the blood bank. The aging of RBCs is associated with the elevation of mechanical fragility (MF) or osmotic fragility (OF) of RBCs, which can lead to cell lysis. The present study was undertaken to identify RBC properties that characte...

Can social instability, food deprivation and food inequality accelerate neuronal aging?

Based on both animal and human studies, inequality in food intake and social instability has adverse effects on the health of individuals and the community. However, it is not known whether social instability, food deprivation and food inequality affect neuronal death and premature aging in young animals. To address this question, the effects of these adverse situations, histopathological chang...

Uncoupling Protein, UCP-4 May Be Involved in Neuronal Defects During Aging and Resistance to Pathogens in Caenorhabditis elegans

Uncoupling proteins (UCPs) are mitochondrial inner membrane proteins that function to dissipate proton motive force and mitochondrial membrane potential. One UCP has been identified in Caenorhabditis elegans (C. elegans), namely UCP-4. In this study, we examined its expression and localization using a GFP marker in C. elegans. ucp-4 was expressed throughout the body from early embryo to aged ad...