Topic: age-related memory impairment

Due to the complexity of CNS, studying the aging processes at the level of neural circuits and individually identified neurons is not an easy task in vertebrates, hence aging research heavily relies on invertebrate models. One such model is the great pond snail (Lymnaea stagnalis), which has been used extensively to study cognitive aging.We made the neuronal transcriptome assembly of Lymnaea and identified several evolutionarily conserved homolog sequences to genes involved in aging, age-related memory impairment, and neurodegenerative diseases of vertebrates including humans. Using young (3-4

The brain, particularly the hippocampus, is sensitive to age-related cellular changes, leading to cognitive deficits. Recent work by our laboratory has demonstrated that autophagy, a catabolic lysosomal-dependant process, is reduced in aged hippocampal neurons, and that restoring autophagy levels is sufficient to improve age-related memory impairment. Nonetheless, the regulatory mechanisms involved in neuronal autophagy decline during aging remain largely unknown. Exploring this question, we found that WD repeat domain phosphoinositide-interacting protein 2 (WIPI2), an important driver of auto

Neurofilaments, neuron-specific cytoskeletal proteins, are heteropolymers composed of four subunits: NFL, NFM, NFH, and αINTX. The synaptic population (SNFs) differs from the axonal subgroup and subserves unique functions, such as the maintenance of synaptic integrity and the modulation of neurotransmission. During aging, synapses undergo several modifications, contributing to the worsening of cognitive performances and the so-called age-related memory impairment. Despite that, nothing is known about "senescent" SNFs. Our research aimed to study the age-related expression pattern of SNFs subun