ePoster

CELLULAR AND MOLECULAR FOOTPRINT OF AGING IN A DEFINED NEURONAL NETWORK ENCODING ASSOCIATIVE MEMORY

István Fodorand 8 co-authors

HUN-REN Balaton Limnological Research Institute

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-046

Presentation

Date TBA

Board: PS02-07PM-046

Poster preview

CELLULAR AND MOLECULAR FOOTPRINT OF AGING IN A DEFINED NEURONAL NETWORK ENCODING ASSOCIATIVE MEMORY poster preview

Event Information

Poster Board

PS02-07PM-046

Abstract

Due to the complexity of the CNS, studying aging in vertebrates at the level of neural circuits and individually identified neurons is challenging. Consequently, aging research often relies on invertebrate models. The great pond snail (Lymnaea stagnalis) has been used extensively for decades to study cognitive aging using an integrative, top-down approach.

We assembled the neuronal transcriptome of Lymnaea and identified several evolutionarily conserved homologs of genes involved in aging, age-related memory impairment, and neurodegenerative diseases in vertebrates, including humans. We hypothesize that the proteins encoded by these sequences are involved in age-related impairments of learning mechanisms in Lymnaea. Using young (3-4-month) and old (11-12-month) snails, we investigated age-related cellular and molecular changes in the whole CNS and in the CGC, a key interneuron involved in implicit learning. In the whole CNS, the expression of 960 transcripts significantly changed during aging, including an age-related decline in molecules critical for learning (e.g., CREB-binding protein). In the CGC, 143 transcripts showed age-dependent expression changes. LC-MS-based untargeted lipidomics identified 291 lipids in the CNS, of which 79 changed significantly with age. Aging was associated with increased polyunsaturated fatty acids, decreased diacylglycerols, and a phospholipid–lysophospholipid shift, suggesting altered membrane fluidity and signaling. LC-MS-based proteomics also revealed age-dependent protein changes (evaluation ongoing).

The identified cellular and molecular changes both at the system and single-cell levels may contribute to age-related memory impairment and highlight conserved mechanisms of cognitive aging relevant beyond mollusks.

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