Topic: engram cells

Achieving early diagnosis in Alzheimer's disease (AD) is a crucial objective in preclinical and clinical AD research, since it represents a therapeutic window during which interventions can be initiated before the onset of severe cognitive decline. Accumulation of amyloid-beta (Aß) in the prefrontal cortex is linked to rapid forgetting in this prodromal AD stage. Thus, early forgetting becomes a potential target for preclinical studies seeking to prevent/delay the onset of severe forms of AD. We used mouse models to identify early alterations in memory formation. Our findings indicate that Aβ1

The interaction between sleep function and memory processing is widely observed in both animals and humans, especially in how sleep supports memory consolidation and forgetting. However, whether memory activity during sleep has any regulatory effect on sleep processes is poorly investigated. Here we find that sensory stimuli-triggered emotional memory reactivation significantly affects sleep strategies after learning, as negative memory promotes alertness in sleep while positive memory protects sleep from perturbation. By combining EEG/EMG recording and engram cell activity tracing, our data r

The panic of losing your car in the carpark captures the importance of associative recognition memory, i.e. the ability to identify something as familiar, along with where and when it was last seen. However, the neuronal networks underpinning this memory are only just being identified. Effectively modelled through object-in-place (OIP) tasks, associative recognition memory can be represented by the time mice spend exploring novel compared to familiar objects and configurations. During learning, active neurons are recruited into neuronal ensembles making an engram, the neural representation of

Alzheimer's Disease (AD), responsible for the majority of dementia cases, is a progressive neurodegenerative disorder marked by amyloid-β accumulation, tauopathy, neuroinflammation, and cognitive decline. Parallel to this cognitive decline, the number of memory-related neurons (engram cells) is reduced in the APPswe/PSEN1dE9 mouse model for slow-progressing AD, crossed with a genetically modified mouse line that allows us to visualize engram neurons (Arc::dVenus mice). We hypothesize that aberrant microglial modulation of engram cells might contribute to the AD-related changes in engram and co

Alzheimer Disease (AD) is the most prevalent form of dementia, and treatments aiming to counteract its effects are missing. Recently, neurons responsible for memory formation (i.e., engrams cells) have been shown to be impaired in mouse models of AD, but no sustained means to rescue their function, and thereby mnemonic capacities are available to date. While partial cellular reprogramming through induction of the Yamanaka Factors (Oct-4, Sox-2, Klf-4 and c-Myc – OSKM) has recently emerged as a promising tool to counteract the systemic effects of aging, reprogramming of specific cell types or i

The amygdala is a brain region primarily associated with emotional response. For example, fear learning and memory are known to activate neurons in the amygdala, which induce gene expression to strengthen the formation of stable engrams. Single-cell transcriptomics can provide insights into behavior-associated cell state changes. Here we present a detailed cell-type taxonomy of the adult mouse amygdala during fear learning and memory consolidation. We perform single-cell RNA sequencing on naïve and fear-conditioned mice, identify 130 neuronal cell types and validate their spatial distributions

Sleep deprivation (SD) negatively affects memory processes, particularly in the hippocampus. Previous research indicates that 6 hours of SD post-learning causes amnesia in hippocampus-dependent tasks. However, we recently demonstrated that object-location memories (OLMs) formed under SD conditions can be effectively recalled several days later using optogenetic engram reactivation or administration of the PDE4 inhibitor roflumilast. These findings suggest that these memories are not lost, but merely difficult to retrieve.Since both cAMP and cGMP signalling critically contribute to memory proce

Epileptogenesis, arising from alterations in synaptic strength, shares mechanistic and phenotypic parallels with memory formation. However, direct evidence supporting the existence of seizure memory remains scarce. We developed a novel conditioned seizure memory (CSM) paradigm, in which seizures and specific cues were paired. The CSM could be reliably retrieved, demonstrating a robust association. We also found that activation of cue-responding engram cells in hippocampus DG could create artificial CSM. After seizure memory retrieval, a protein synthesis-dependent reconsolidation process invol

Memory is the capacity of an organism to acquire, store and recover information based on experience. In the brain, experiences that become memories appear as enduring changes only in a small set of activated neurons, called engrams.While the mechanisms of how such memories are deposited in engrams for short periods of time has received considerable attention over the past decade, the current knowledge of how memories are stored in engram cells in the long run is still scarce. Consequently, this project aims to identify the mechanisms based on which a memory becomes remote by integrating a wide