Alaattin Kaya

This study shows C. elegans uses chromoprotein photosensitization and bacterial metabolic cues to prefer red over blue food, independent of light and photoreceptors.

This study shows that NPC1 deficiency causes genomic instability and immune activation linked to neurodegeneration and aging, and identifies Fingolimod as a potential treatment.

This paper shows that manipulating intracellular ATP levels in yeast through synthetic ATP import extends cellular lifespan and reveals distinct metabolic pathways involved in aging.

The paper measures mTORC1 activity via phosphorylated p70S6K in psychiatric patients and finds it correlates with body structure and medication response to ketamine and rapamycin.

This study identifies molecular factors and pathways associated with genotype-dependent lifespan variation in response to caloric restriction in wild yeast isolates.

The paper investigates proteome and transcriptome changes in Alzheimer's disease brains and identifies a stem cell-derived extracellular vesicle subpopulation with therapeutic potential for mitochondrial proteostasis and inflammation.

The paper identifies a Niemann-Pick type C mouse model with accelerated brain aging as a novel model for Alzheimer's disease research by analyzing transcriptomic data from congenital diseases.

The paper identifies common molecular signatures between coronavirus infection and Alzheimer's disease to suggest potential therapeutic targets.

The paper investigates how knocking out nuclear-encoded mitochondrial genes in yeast affects lifespan, revealing shared mechanisms involving ribosomal proteins, actin dynamics, and proteasome function.

Rapamycin treatment during early life extends lifespan and healthspan in mice and Daphnia magna by slowing development and delaying aging.

The paper analyzes lifespan variation in wild yeast isolates to identify genetic and environmental factors shaping replicative lifespan and cellular processes involved in aging.