Volume 1 Issue 4, April 2021

The latest spat over the potential approval of aducanumab, an amyloid-β-targeting drug for Alzheimer’s disease, highlights continuing controversy over the amyloid-β hypothesis.

There is a major and rapidly growing deficiency in the US eldercare workforce at all levels, especially among physicians. Efforts to increase recruitment and retention into geriatrics have failed, especially among critically important educators and researchers. Possible strategies to assure adequate care for older persons are discussed.

Groh and colleagues investigate the age-related degeneration of axons in the optic nerve and other brain regions and show that at least part of this degeneration is due to the presence of T cells.

Using mouse models of osteoarthritis (OA), a new study finds that osteoclasts secrete exosomes that deliver miRNAs to chondrocytes, leading to an increase in metalloproteinase activity in cartilage. A bone-specific inhibitor of exosome production can halt this process, hinting at a new therapeutic strategy for patients with OA.

In this Perspective, McMahon et al. examine the emerging roles and implications of post-transcriptional RNA modifications, or the epitranscriptome, in aging and age-related diseases, highlighting potential epitranscriptomic mechanisms and/or their dysfunction that may regulate the aging process.

Polypharmacy is a leading health concern entangled with many geriatric syndromes. This Review provides an overview of the current research landscape and a critical appraisal of existing and emerging approaches to address polypharmacy.

Aging is accompanied by structural and functional alterations of the central nervous system (CNS). Here, the authors show that cytotoxic CD8⁺ T cells accumulate in the CNS during normal aging, leading to axonal damage and contributing to age-related cognitive and motor decline.

The authors show that exosomal transfer of osteoclast-derived microRNAs to chondrocytes decreases the resistance of cartilage to matrix degeneration, angiogenesis and sensory innervation, and promotes osteoarthritis progression in mice.

Microglia can help clear amyloid β plaques in the Alzheimer’s disease brain but may also become dysfunctional and can contribute to disease progression. March-Diaz et al. reveal that hypoxia, a potentially modifiable risk factor for Alzheimer’s disease, disrupts the metabolism and function of microglia near plaques, which may contribute to neuropathology.

Using genetic and demographic data from the UK Biobank, the authors clustered 116 common diseases based on their age-of-onset profiles and found increased genetic similarity within clusters, suggesting common etiologies. Two of the four disease clusters were associated with aging-related genes but differed in functional enrichment and evolutionary profiles.