Aging

An in-person Stanford symposium highlighting recent progress in brain resilience and aging research, followed by a neuroscience poster session featuring work from the Stanford community.

Establish an independent research programme on the cellular and molecular biology of aging in humans or model systems. Relevant topics include senescence, protein homeostasis, metabolism, mitochondrial biology, genome stability, epigenetic regulation, stem cells and the neurobiology of aging. The appointment includes teaching, mentoring, collaborative research and university service. Priority review is 15 November 2026.

…methods, drug discovery, imaging, neuroscience, aging, nanobiotechnology, quantum biology and artificial intelligence. Hosted by the University of Waterloo with the University of Guelph and Wilfrid Laurier University, the in-person programme is expected to include a trainee symposium, invited and contributed talks, posters, professional development and industry engagement. Teaching, science communication and public engagement will also feature.

…in Alzheimer’s disease and aging.

Develop sequence-based deep-learning models of gene regulation and aging. Research predicts gene expression and chromatin accessibility from DNA, interprets genetic variation and connects model predictions with experiments, causal mechanisms and possible intervention points.

…plasticity, development, genetics and aging. Experimental, computational, cellular and non-model-organism approaches are welcome. The appointee develops interdisciplinary collaborations across biology and neuroscience, teaches and mentors students, and contributes university service. Application review begins 1 December 2026 and continues until filled.

Neighborhood conditions influence health and aging, but researchers can face difficulties finding contextual measures and combining them with their own studies. This practical workshop introduces NaNDA, a free archive of neighborhood measures covering the United States over several decades. Participants will work through dataset selection, geographic identifiers, matching time periods, and linkage to survey or administrative data. The programme includes a repository tour, aging-research examples, beginner and intermediate breakout groups, and discussion of participants’ data-linkage questions.

Promoting adult neurogenesis in aging has the potential to rejuvenate neural circuits and restore associated functions. Establishing tractable models of adult neurogenesis can significantly expedite the identification of compounds and their cellular mechanisms promoting nervous system regeneration in aging. We have established the fruit fly Drosophila melanogaster as an easily scalable, highly tractable and genetically conserved platform to analyze nervous system regeneration. Particularly, by developing and implementing genetically-encoded lineage tracing systems, as well as molecular and ima

Aging is characterized by impairments in decision-making, memory, and learning. Classical theories suggest that the cognitive decline may be caused by increased neural variability, reducing the signal-to-noise ratio of information processing in the central nervous system. To explicitly test this hypothesis, we investigate behavior and brain activity in young and old mice performing a visual decision-making task. Old animals show relatively worse performance (a shallower psychometric curve and slower reaction times). We then used extracellular neural recordings to quantify single-neuron variabi

Aging is associated with the slowdown of neuronal processing and cognitive performance in the brain; however, the exact cellular mechanisms behind this deterioration in humans are poorly elucidated. Recordings in human acute brain slices prepared from tissue resected during brain surgery enable the investigation of neuronal changes with age. Although neocortical fast-spiking cells are widely implicated in neuronal network activities underlying cognitive processes, they are vulnerable to neurodegeneration. Herein, we analyzed the electrical properties of 147 fast-spiking interneurons in neocort

…readouts, stimuli, and genetic/aging contexts and use this to build an atlas and m

Aging-correlated cognitive declines, including deficiencies in spatial orientation and memory, may reflect dysfunction in the hippocampus and medial entorhinal cortex (MEC). However, aging-related changes in MEC at the cellular and molecular levels remain unclear. In this study, we found fewer grid cells with reduced spatial stability in old mice. We compared gene expression profiles between young and old mice using 10x Genomics Visium technology. Among 1664 differentially expressed genes, we discovered a marker gene for subpopulation in MEC Layer III with decreased cell number with age. Silen

Aging and neurodegenerative diseases, such as Alzheimer's (AD) or Amyotrophic Lateral Sclerosis (ALS), led to widespread degeneration of long-range connections in cortical structural connectivity (SC). These damages manifest as losses in connections or demyelination of axons. When the SC of the brain is damaged, the functional connectivity (FC, i.e. the dynamic interactions and information exchange between distinct brain regions) is locally and globally perturbed. Despite the close correlation between SC and FC, they are not identical; FC exhibits greater flexibility and can reorganize in resp

Learning whom to trust is an important social skill, which can be affected by aging and loneliness. An often-used experimental task to study trust learning is the repeated trust game (Berg et al., 1995) where participants repeatedly invest money in another player who can be trustworthy – or not. 50 healthy, neurotypical older adults (64 to 84 years) and 62 younger adults (age: 20 to 33, see Sladky & Riva et al., 2022) played the repeated trust game (Figure 1a) while undergoing 3T functional MRI. We found that trust learning was impaired in older adults, particularly in those who reported h

Calorie restriction (CR) is recognized for its potential to delay age-related changes; however, its effectiveness can vary based on factors such as duration, age, and sex. Implementing CR later in life may not only diminish its protective potential but could also have detrimental effects. Herein, we aimed to investigate the effect of CR on short-term (STM) and long-term (STM) memory and explore the potential role of the mTOR signaling pathway as an underlying molecular mechanism. Female Wistar rats of different ages (adult, middle-aged, and old) were exposed to CR (60% of ad libitum (AL)) to s

Aging, both physiological and pathological, results in a widespread decline in cognitive, sensory, and motor functions. Adult hippocampal neurogenesis is a phenomenon that diminishes with age across various mammalian species and has been proposed as a significant factor linked to age-related cognitive deficits. Our laboratory's preliminary studies reveal that mice lacking the DREAM protein (dream -/-) exhibit cognitive improvement with aging, along with increased neurogenesis and greater development of immature neurons positive for DCX compared to wild-type mice of the same age. To further und

Endurance training can improve cognitive function in aging people. It seems related to the expression of neurotrophic factors stimulating neurogenesis in the hippocampus and synaptic plasticity in the cortex and/or hippocampus. However, the benefits are highly dependent on the duration, intensity and frequency of exercise, which remains to determine. The aim of the current study is to compare 4 weeks of either high-intensity interval (HIIT) or moderate-intensity continuous (MICT) training on cognition, endurance and sensorimotor performance, and neuroplasticity markers. For that, 24 aged rats

The negative impact of aging on the vestibular system and the integration of vestibular inputs by the central nervous system can potentially worsen the lack of vestibular input in areas related to cognition, leading to a decline in cognitive function. Galvanic Vestibular Stimulation (GVS) is a non-invasive method that uses weak electrical currents to stimulate the vestibular system through electrodes placed over the mastoid processes. This study aimed to investigate whether GVS may improve cognitive performance in healthy older adults. Twenty-one subjects (12 female, age: 64.6 ± 2.9) were rand

Recent evidence suggests that epigenetic mechanisms may contribute to memory deficits in aging. Specifically, in the hippocampus, the repressive epigenetic mark H3K9me3 (tri-methylated lysine 9 on histone H3) has been implicated in the silencing of genes essential for memory. Yet, the impact of the age-related increased H3K9me3 levels on neuronal function remains unclear. We hypothesized that H3K9me3 accumulation renders neurons refractory to stimulation. To assess the influence of H3K9me3 on neuronal activation, we reduced H3K9me3 levels by silencing the major methyltransferase responsible to

Metabolic cost for the nervous system is very high due to the complexity of neuronal morphology and the processes to sustain neuronal transmission and synaptic plasticity. Cognitive functions underlying complex behaviors further increase brain energy demands. Despite the interest given to brain metabolism during the last years, how modification of metabolism might contribute to cognitive dysfunctions in brain disorders is not clear. Thus, we aim to identify the key metabolic pathways activated during complex cognitive functions. In this study, we will focus on metabolic pathways activated by d

Aging leads to the accumulation of misfolded proteins, such as β-amyloid and α-synuclein, which are believed to underly the onset of neurodegenerative disorders. Most of the treatments for brain disorders come from pre-clinical evidence in males, although women are more vulnerable than men to Alzheimer’ disease (AD) which is the first cause of age-related dementia. However, the mechanisms underlying these sex-differences are not known.To date, two therapeutic approaches are predominantly used to prevent and/or slow neurodegeneration; they include autophagy pharmacological enhancers and exercis

Aging is a multifactorial process characterized by the slow decline of cellular physiology associated with a lowdown of brain functions. Neurological complications mainly reflect defects at the synaptic structure. Indeed, preclinical studies demonstrate that preserving functionality of synapses delays the occurrence of aged-related neurological and cognitive defects and prevents the progressive neuronal degeneration. Since defects in DNA repair mechanisms have a critical role in aged-related neurological diseases and expression of core DNA repair genes is downregulated during aging across brai

…trajectories of mitophagy within the aging mammalian brain remain unexplored. We profiled mitophagy and macroautophagy within intact brain tissues using advanced genetically-encoded optical reporter mice. Methods: We an

Aging has potent effects on many basic parameters of circadian rhythm and also are associated with impairments in learning and memory. Melatonin, a hormone mainly secreted in the pineal gland, is believed to restore circadian rhythm of clock genes in the suprachiasmatic nucleus during aging. The present study attempted to examine the daily profiles of different clock genes, and the clock-controlled cognition-related gene during development and aging and examine the effect of melatonin on the expression of these genes during aging in rat hippocampus. The results showed that the mRNA of the cloc