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How does memory formation work in the brain? ​

Abstract ​

Memory formation is a fundamental cognitive process essential for learning and personal identity, involving intricate neural mechanisms and structures such as the hippocampus, amygdala, and neocortex. This review synthesizes current knowledge on memory types, distinguishing between declarative and non-declarative memory, and explores the key brain structures involved in memory formation. Declarative memory, reliant on the hippocampus and medial temporal lobe, enables conscious recollection of facts and events, while non-declarative memory encompasses unconscious skills and habits mediated by different brain regions. Molecular mechanisms, particularly synaptic plasticity, are crucial for memory encoding and consolidation, with neurotransmitters and hormones modulating these processes. Recent advancements in neuroimaging techniques, including fMRI and PET scans, have enhanced our understanding of the neural correlates of memory tasks, revealing dynamic interactions between brain regions during memory processes. The implications of these findings are significant for addressing memory-related disorders, such as Alzheimer's disease and PTSD, emphasizing the importance of understanding the neurobiological underpinnings of memory. This comprehensive overview highlights the complexity of memory formation and suggests future research directions aimed at developing effective interventions for cognitive impairments.

Outline ​

This report will discuss the following questions.

  • 1 引言
  • 2 Overview of Memory Types
    • 2.1 Declarative Memory
    • 2.2 Non-Declarative Memory
  • 3 Key Brain Structures Involved in Memory Formation
    • 3.1 The Hippocampus
    • 3.2 The Amygdala
    • 3.3 The Neocortex
  • 4 Molecular and Cellular Mechanisms of Memory
    • 4.1 Synaptic Plasticity
    • 4.2 Role of Neurotransmitters
    • 4.3 Hormonal Influences on Memory
  • 5 Advances in Neuroimaging Techniques
    • 5.1 Functional MRI
    • 5.2 PET Scans
    • 5.3 Electrophysiological Techniques
  • 6 Implications for Memory Disorders
    • 6.1 Alzheimer's Disease
    • 6.2 PTSD
    • 6.3 Other Memory-Related Conditions
  • 3 总结

1 Introduction ​

Memory formation is a fundamental cognitive process that underpins learning, adaptation, and the continuity of personal identity. Understanding how memories are created, stored, and retrieved has captivated neuroscientists for decades, as it not only sheds light on the intricate workings of the brain but also holds significant implications for addressing memory-related disorders. Memory formation involves a myriad of neural mechanisms and structures, with the hippocampus, amygdala, and neocortex playing pivotal roles. The complexity of these processes is underscored by the interplay of molecular and cellular mechanisms, particularly synaptic plasticity, which is essential for memory encoding and consolidation.

The significance of studying memory formation extends beyond mere academic curiosity; it has profound implications for treating conditions such as Alzheimer's disease, post-traumatic stress disorder (PTSD), and other memory-related conditions. As we continue to unravel the neurobiological underpinnings of memory, we gain insights into potential therapeutic targets that could ameliorate cognitive impairments associated with these disorders. For instance, the role of neurotransmitters and hormones in modulating memory processes is an area of active investigation, revealing pathways that could be harnessed for pharmacological interventions [1].

Current research has established that memory can be categorized into different types, primarily declarative and non-declarative memory. Declarative memory encompasses the conscious recollection of facts and events, while non-declarative memory involves skills and habits that are often performed unconsciously. Understanding the distinctions between these memory types is crucial for elucidating the diverse mechanisms that govern memory formation. For example, studies have demonstrated that the amygdala is integral to emotional memory, highlighting the role of emotional states in the retention and accuracy of memories [2].

Recent advancements in neuroimaging techniques have further enhanced our understanding of memory formation. Functional MRI (fMRI), positron emission tomography (PET), and electrophysiological methods have allowed researchers to visualize brain activity associated with memory tasks, leading to new insights into the dynamic processes underlying memory consolidation and retrieval [3]. These techniques have also facilitated the exploration of the neural circuitry involved in memory, revealing how different brain regions interact during the formation of memories [4].

This review is organized to provide a comprehensive overview of memory formation in the brain. We will first delineate the various types of memory, emphasizing the differences between declarative and non-declarative memory. Next, we will explore the key brain structures involved in memory formation, including the hippocampus, amygdala, and neocortex. Following this, we will delve into the molecular and cellular mechanisms that facilitate memory, focusing on synaptic plasticity, the roles of neurotransmitters, and hormonal influences. The review will also highlight recent advancements in neuroimaging techniques that have revolutionized our understanding of memory processes. Finally, we will discuss the implications of these findings for memory-related disorders, particularly focusing on conditions such as Alzheimer's disease and PTSD.

In conclusion, by synthesizing current knowledge in the field of memory formation, this review aims to provide a holistic understanding of the intricate biological processes that govern memory, addressing both fundamental principles and emerging research trends. As we continue to unravel the complexities of memory, we move closer to developing effective interventions for those affected by memory impairments, ultimately enhancing our understanding of the human brain and its remarkable capabilities.

2 Overview of Memory Types ​

2.1 Declarative Memory ​

Memory formation in the brain, particularly declarative memory, involves a complex interplay of various brain regions, notably the hippocampus, medial temporal lobe, and the neocortex. Declarative memory is characterized by the ability to recall facts and events and is distinct from other forms of memory due to its reliance on specific neural mechanisms.

Declarative memory is primarily mediated by a brain system that includes areas of the cerebral cortex and the hippocampal region. This system facilitates distinct functional contributions to memory processing, which allows for the organization of memories in ways that support the unique properties of declarative memory expression. Eichenbaum (1997) highlights that the discovery of declarative memory as a distinct category represents a significant achievement in cognitive science, emphasizing its underlying brain mechanisms [5].

The hippocampus is often regarded as a critical component of the declarative memory system, traditionally viewed as a module dedicated to the formation of conscious memories. However, recent research suggests that the hippocampus plays a broader role in cognition, contributing to various memory processes beyond just declarative memory. Shohamy and Turk-Browne (2013) propose that the hippocampus interacts with other brain systems and cognitive processes through two mechanisms: the memory modulation hypothesis and the adaptive function hypothesis. These mechanisms illustrate how the hippocampus can modulate mnemonic representations and support both mnemonic and non-mnemonic functions [6].

The process of memory formation can be understood at a system level, where encoding transforms perceptual representations into enduring memories. Fernández and Tendolkar (2001) describe how functional imaging studies have identified specific regions in the medial temporal and prefrontal areas that exhibit heightened neural activity during successful memory formation. This indicates that distinct mnemonic operations occur in the medial temporal lobe, integrated with semantic and perceptual operations in the prefrontal cortex [7].

Moreover, the formation of memories involves not only structural changes in synaptic connections but also potential chemical mechanisms. Peña De Ortiz and Arshavsky (2001) propose that permanent memory might have a chemical basis, suggesting that memory coding mechanisms in the brain could be analogous to those in the immune system, potentially involving somatic recombination processes [8].

In summary, declarative memory formation is supported by a network of brain regions, primarily the hippocampus and medial temporal lobe, which work in conjunction with the neocortex. These areas are involved in various processes, including encoding, consolidation, and retrieval of memories, characterized by both structural and potential chemical modifications. The understanding of these mechanisms continues to evolve, highlighting the complexity and interconnectivity of memory systems within the brain.

2.2 Non-Declarative Memory ​

Memory formation in the brain involves complex processes that are mediated by various neural structures and mechanisms. The understanding of memory has evolved significantly, leading to the recognition of distinct types of memory systems, including declarative and non-declarative memory.

Declarative memory, often referred to as explicit memory, is the system responsible for the conscious recollection of facts and events. This type of memory relies heavily on the hippocampus and surrounding medial temporal lobe structures, which have been identified as critical for the encoding and retrieval of declarative memories. Eichenbaum (1997) emphasizes that declarative memory is supported by a specific brain system, which includes areas of the cerebral cortex and the hippocampal region, each contributing uniquely to memory processing[5].

In contrast, non-declarative memory encompasses a variety of unconscious memory systems that include skills, habits, and conditioned responses. This type of memory is not reliant on the hippocampus and instead involves different brain regions such as the striatum, cerebellum, and amygdala. Squire and Zola (1996) discuss how non-declarative memory can be assessed through various tasks that evaluate classification learning, perceptuomotor skills, and other implicit learning processes[9].

Recent research has revealed that the hippocampus plays a broader role in cognition beyond just declarative memory. Shohamy and Turk-Browne (2013) propose a theoretical framework suggesting that the hippocampus interacts with other brain systems in two main ways: through the memory modulation hypothesis, where mnemonic representations in the hippocampus influence the operation of other cognitive systems, and the adaptive function hypothesis, which posits that the hippocampus contributes to both mnemonic and non-mnemonic functions[6].

Memory formation is not only about the storage of information but also involves dynamic remodeling of synaptic connections between neurons. The cellular mechanisms underlying these dynamics are still being elucidated. For instance, Zaki and Cai (2020) highlight the role of microglia in regulating synaptic formation by clearing extracellular matrix proteins, which is essential for memory formation[10].

In summary, memory formation in the brain is a multifaceted process that includes both declarative and non-declarative memory systems, each supported by distinct neural structures and mechanisms. While declarative memory is linked to conscious recollection and relies on the hippocampus, non-declarative memory encompasses a range of implicit processes governed by different brain regions. The interactions and dynamics of these memory systems continue to be an active area of research, providing deeper insights into how the brain encodes, stores, and retrieves memories.

3 Key Brain Structures Involved in Memory Formation ​

3.1 The Hippocampus ​

The hippocampus is a critical brain structure involved in the processes of memory formation and consolidation. Its role is multifaceted, encompassing various types of memory, including declarative and episodic memories. The hippocampus operates through mechanisms such as synaptic plasticity, particularly long-term potentiation (LTP), which is essential for the consolidation of memories.

Research has demonstrated that the hippocampus acts as a temporary buffer for memories, facilitating their transition to long-term storage in the neocortex. This concept is supported by the findings from lesion studies in humans and animal models, which indicate that damage to the hippocampus results in significant memory impairments, particularly in forming new episodic memories. For instance, the famous case of patient H.M. illustrated the hippocampus's crucial role in memory formation, as this individual exhibited profound anterograde amnesia following surgical removal of parts of the medial temporal lobe, including the hippocampus [11].

The hippocampus is not solely responsible for the encoding and retrieval of memories; it also interacts with other brain regions. Recent studies suggest that different subregions of the hippocampus are differentially involved in encoding and retrieval processes. For example, the dentate gyrus and CA fields 2 and 3 are more active during episodic memory formation, while the subiculum is primarily involved in the recollection of previously learned episodes [12].

Moreover, the hippocampus is implicated in spatial navigation and memory, as evidenced by the discovery of "place cells" that activate when an individual is in a specific location, suggesting that the hippocampus serves as a cognitive map for spatial orientation [11]. This spatial processing capability complements its role in associating complex multimodal information, thereby facilitating the formation of new memory traces [13].

The neurogenesis occurring within the hippocampus also plays a significant role in memory formation. Adult-born neurons contribute to hippocampal-dependent cognitive functions, although the relationship between neurogenesis and learning remains complex and context-dependent [14]. Factors such as stress levels, age, and previous experiences can modulate neurogenesis and, consequently, memory capabilities [14].

Cholecystokinin (CCK) has been identified as a modulator in hippocampal neuroplasticity and memory formation, facilitating LTP and influencing the circuitry within the hippocampus [4]. This underscores the complexity of the mechanisms involved in memory formation, highlighting the interplay between various neurotransmitters, hormones, and neuroplastic changes in the hippocampus.

In summary, the hippocampus is a pivotal structure for memory formation, functioning through intricate mechanisms of synaptic plasticity, neurogenesis, and interaction with other brain regions. Its roles encompass not only the consolidation of memories but also spatial navigation and the integration of diverse information types, making it essential for both declarative and episodic memory processes.

3.2 The Amygdala ​

Memory formation in the brain involves a complex interplay of various structures, among which the amygdala plays a crucial role, particularly in the context of emotional memories. The amygdala, located in the temporal lobe, is integral to emotional responses and the consolidation of emotional memories. It interacts dynamically with other brain regions, notably the hippocampus, to enhance memory retention and retrieval.

The amygdala is known to facilitate synaptic plasticity in other brain structures, such as the hippocampus and basal ganglia, which are believed to serve as storage sites for various types of memory. In emotionally charged situations, the amygdala enhances the processing of incoming information, allowing it to be integrated more effectively within the broader cerebral networks responsible for memory formation. This suggests that emotional conditions can lead to long-term neural plasticity within the amygdala, influencing how it modulates memory-related processes in the hippocampus and other areas of the brain (Paz & Pare, 2013) [15].

The basolateral amygdala (BLA) is particularly significant in the context of long-term fear memory formation. It has been shown that the activation of the BLA is influenced by stress hormones and various neuromodulatory systems, which converge to regulate noradrenaline-receptor activity. This activation is essential for modulating memory consolidation, as the BLA sends projections to multiple brain regions, including the hippocampus, which are involved in establishing lasting memories (McGaugh, 2002) [16].

Recent research utilizing spatial and single-cell transcriptomics has provided insights into the cellular and molecular architecture of the BLA's role in long-term memory. It has been identified that specific transcriptional signatures in neurons and astrocytes associated with memory persist for weeks. These changes implicate neuropeptide signaling, MAPK and CREB activation, and synaptic connectivity as key components in the formation of long-term memory (Sun et al., 2024) [17].

Moreover, the interaction between the amygdala and hippocampus is not static; it is influenced by the emotional history of the individual. The amygdala's role in emotional memory formation can be viewed from two perspectives: it either modulates memory processes in other brain regions or serves as a site for certain aspects of emotional memory itself. This dual function adds complexity to our understanding of how emotional experiences are encoded into long-term memories (Richter-Levin, 2004) [18].

In summary, the amygdala is essential for the formation of emotional memories, acting through a dynamic interplay with the hippocampus and other brain regions. Its role in enhancing synaptic plasticity and memory consolidation highlights the importance of emotional context in memory formation, underscoring the intricate relationship between emotion and cognition in the brain.

3.3 The Neocortex ​

Memory formation in the brain involves a complex interplay of various structures, with the neocortex playing a crucial role in the process. The neocortex is integral to higher-order brain functions, including cognition, sensory perception, and motor control. It is primarily responsible for the long-term storage of memories, particularly after the initial encoding phase that occurs in the hippocampus.

The medial temporal lobe, which includes the hippocampus and adjacent cortical structures such as the entorhinal, perirhinal, and parahippocampal cortices, is essential for declarative memory—conscious memory for facts and events. This system works in conjunction with the neocortex to establish and maintain long-term memories. Initially, memories are dependent on the hippocampus for encoding, but as time progresses, these memories become increasingly consolidated and eventually independent of the hippocampus, residing primarily in the neocortex [19].

Research has demonstrated that the formation of new memories is reliant on the hippocampus and adjacent cortex, with final storage believed to occur within a distributed network across the neocortex. This process is supported by evidence from functional neuroimaging studies and electrophysiological recordings that reveal how widespread neocortical networks activate during memory consolidation [20].

Moreover, the process of systems consolidation describes how the hippocampus facilitates the reorganization of information stored in the neocortex, allowing it to become independent over time. This is particularly evident in studies of retrograde amnesia, which show that damage to the hippocampus impairs more recent memories while sparing older ones, suggesting that older memories have undergone consolidation and are thus less reliant on the hippocampus [21].

In the context of spatial memory, the neocortex also plays a critical role. Studies have identified specific regions within the neocortex, such as the prefrontal and anterior cingulate cortices, as vital for the storage and retrieval of remote spatial memories. This indicates that long-term memory storage is accompanied by structural changes in these neocortical regions, including synaptogenesis and laminar reorganization, as the hippocampus becomes functionally disengaged from the memory process [22].

Overall, the neocortex is not merely a passive storage site but actively participates in the memory formation process, influencing how memories are encoded, consolidated, and retrieved. As such, the interactions between the hippocampus and the neocortex are fundamental to understanding the neurobiological underpinnings of memory formation [23].

In summary, memory formation in the brain involves a dynamic relationship between the hippocampus and the neocortex, where initial encoding occurs in the hippocampus and subsequent consolidation and storage occur in the neocortex. This intricate system underscores the importance of the neocortex in maintaining long-term memories and highlights the ongoing dialogue between these brain regions throughout the memory process.

4 Molecular and Cellular Mechanisms of Memory ​

4.1 Synaptic Plasticity ​

Memory formation in the brain is fundamentally rooted in synaptic plasticity, which refers to the ability of synapses—the connections between neurons—to strengthen or weaken over time in response to increases or decreases in their activity. This process is critical for encoding and storing memories, and it involves various molecular and cellular mechanisms.

At the core of synaptic plasticity is the concept that changes in the strength of synaptic connections are the primary means by which memory traces are encoded in the central nervous system. The synaptic plasticity and memory hypothesis posits that "activity-dependent synaptic plasticity is induced at appropriate synapses during memory formation and is both necessary and sufficient for the information storage underlying the type of memory mediated by the brain area in which that plasticity is observed" (Martin et al. 2000). This hypothesis emphasizes that the dynamic nature of synaptic connections directly influences learning and memory processes.

Research has shown that long-term potentiation (LTP), a long-lasting enhancement in signal transmission between two neurons that results from their repeated and persistent stimulation, plays a crucial role in memory formation. LTP is considered a cellular substrate for learning, particularly in brain regions such as the hippocampus, which is essential for forming new memories (Bruel-Jungerman et al. 2007). Conversely, synaptic weakening, or long-term depression (LTD), is also significant as it can facilitate the removal of outdated or unnecessary memories, highlighting the brain's ability to adapt and reorganize itself.

Recent studies have expanded the understanding of synaptic plasticity beyond the traditional view that primarily focuses on excitatory synapses. Neuromodulatory systems influence synaptic plasticity at various levels, including network, circuit, and synaptic levels, thereby directing information flow and altering synaptic responses based on behavioral states (Fuchsberger & Paulsen 2022). This modulation is crucial for tailoring learning experiences and memory consolidation, as it enables the brain to adjust its responses to environmental stimuli.

Furthermore, epigenetic mechanisms have been identified as critical regulators of synaptic plasticity and memory formation. Modifications such as DNA methylation and histone acetylation and methylation affect gene transcription related to memory processes (Sen 2015). These epigenetic changes can be induced by various stimuli, including drug abuse, and they can lead to long-lasting alterations in gene expression that underpin cognitive functions.

The integration of these findings indicates that memory formation is a complex interplay of synaptic modifications, epigenetic regulation, and the influence of neuromodulatory systems. This multifaceted approach provides a more comprehensive understanding of how memories are encoded, consolidated, and retrieved, ultimately shaping cognitive function and behavior. The study of synaptic plasticity not only enriches the understanding of normal memory processes but also has implications for addressing cognitive disorders and enhancing therapeutic strategies for memory-related conditions (Silva et al. 2000; Roth & Sweatt 2009).

4.2 Role of Neurotransmitters ​

Memory formation in the brain is a complex process that involves various molecular and cellular mechanisms, particularly the roles of neurotransmitters and other signaling pathways. A significant aspect of memory consolidation is the involvement of the central noradrenaline (NA) system, which has been shown to play a crucial role in long-term memory formation. Specifically, the NA system mediates de novo protein synthesis and gene expression necessary for this process, indicating that it is integral to memory consolidation (Kobayashi & Yasoshima, 2001) [24].

Furthermore, the brain's architecture undergoes dynamic remodeling during memory formation, primarily through synaptic plasticity. This remodeling is facilitated by various types of glial cells, particularly microglia, which have recently been identified as key players in regulating synaptic formation. Microglia contribute by clearing extracellular matrix proteins that can impede synaptic connectivity, thus creating a conducive environment for synaptic plasticity and memory formation (Zaki & Cai, 2020) [10].

Astrocytes, another type of glial cell, are also crucial for memory processes. They are involved in energy metabolism, particularly through glycogenolysis and lactate production, which are essential for sustaining the energy demands of neurons during long-term memory formation. The metabolic coupling between astrocytes and neurons facilitates the energy supply necessary for the enduring changes in neuronal function associated with memory (Alberini et al., 2018) [25].

In addition to these cellular interactions, epigenetic mechanisms play a significant role in how memories are encoded and maintained. The field of neuroepigenetics has explored how various modifications, such as histone modification and DNA methylation, dynamically regulate gene expression required for memory formation. These modifications can lead to stable alterations in neuronal function and synaptic structure, which are critical for the persistence of memories (Campbell & Wood, 2019) [26].

Collectively, these findings highlight that memory formation is not solely reliant on neuronal mechanisms but also involves a sophisticated interplay between neurotransmitter systems, glial cells, and epigenetic changes, all of which contribute to the complex landscape of memory encoding, consolidation, and retrieval.

4.3 Hormonal Influences on Memory ​

Memory formation in the brain is a complex process that involves various molecular and cellular mechanisms, as well as hormonal influences. The brain is equipped with both mechanisms that facilitate the formation and retention of memories and those that suppress irrelevant information, ensuring efficient memory management.

At the molecular level, memory formation is heavily reliant on epigenetic regulation, which encompasses processes such as DNA methylation and histone modifications. These epigenetic changes play a crucial role in gene transcription, protein synthesis, and synaptic plasticity, which are essential for the establishment of long-term memories. For instance, the epigenetic machinery regulates the formation and stabilization of long-term memory by modulating gene expression in response to learning experiences. This regulation can be viewed in two ways: a "gating" role where the chromatin state influences activity-triggered gene expression, and a "stabilizing" role that maintains the molecular and cellular changes induced by memory-related events [27].

Recent studies have highlighted the importance of chromatin remodeling in memory regulation. This involves three-dimensional structural changes in chromatin that affect gene regulation, which is vital for learning and memory. Specific epigenetic processes, including DNA methylation, histone methylation, and histone acetylation, have been identified as key players in these mechanisms [28].

Moreover, hormonal influences, particularly from sex-steroid hormones such as 17β-estradiol (E2), have been shown to significantly affect memory processes. Research indicates that E2 enhances memory formation through epigenetic alterations, specifically histone acetylation and DNA methylation in the hippocampus. These hormonal effects on memory consolidation underscore the interaction between hormonal signals and epigenetic mechanisms, suggesting that factors such as environmental enrichment and stress can modulate cognitive function by influencing these epigenetic processes [29][30].

In summary, memory formation in the brain involves a sophisticated interplay of molecular mechanisms, particularly epigenetic regulation, which dictates gene expression and synaptic changes necessary for memory retention. Hormonal influences further modulate these processes, emphasizing the dynamic nature of memory formation and the various factors that can enhance or impair cognitive functions. Understanding these intricate mechanisms provides valuable insights into how memories are formed, stabilized, and retrieved, as well as how disruptions in these processes may lead to memory-related disorders [3][26].

5 Advances in Neuroimaging Techniques ​

5.1 Functional MRI ​

Memory formation in the brain is a complex process that involves various neural structures and mechanisms, which can be elucidated through advancements in neuroimaging techniques, particularly functional magnetic resonance imaging (fMRI). fMRI provides a non-invasive means to study the neural correlates of memory formation by measuring brain activity associated with cognitive tasks.

The hippocampus and prefrontal cortex are critical regions implicated in memory processes. Research indicates that these areas are involved in successful associative encoding, which is essential for forming new memories. For instance, fMRI studies have shown that patients with Alzheimer's disease exhibit decreased activation in the hippocampus and related medial temporal lobe structures during the encoding of new memories, compared to cognitively intact older adults. This suggests that the integrity of these regions is vital for memory formation and retrieval (Sperling 2007) [31].

Moreover, the relationship between brain activity and memory strength appears to be nonlinear, differing between the hippocampus and perirhinal cortex. Studies have demonstrated that the hippocampus shows a positively accelerated function concerning memory strength, while the perirhinal cortex displays a negatively accelerated function. This indicates that while both structures contribute to memory, they do so in distinct ways, which can affect how memories are formed and recalled (Song et al. 2011) [32].

Functional MRI has also been employed to explore the effects of learning on brain activation patterns. For example, a study involving healthy participants found significant differences in brain activation across various regions, particularly in the occipital and temporal lobes, during memory tasks following intensive learning. This highlights the role of specific brain structures in supporting different types of cognitive functions, including learning and memory (Ahmed-Popova et al. 2020) [33].

Furthermore, mood can significantly influence memory formation, as evidenced by fMRI studies that explore mood-congruent memory biases. These studies reveal that emotional states can modulate the neural mechanisms underlying memory encoding and retrieval, particularly through interactions in the prefrontal cortex and the medial temporal lobe (Fitzgerald et al. 2011) [34].

In summary, memory formation in the brain is facilitated by a network of regions, with the hippocampus and prefrontal cortex playing central roles. Advances in fMRI have provided insights into the dynamics of memory processes, revealing the nonlinear relationships between brain activity and memory strength, the impact of learning, and the influence of emotional states on memory encoding and retrieval. These findings underscore the intricate interplay between various cognitive processes and the underlying neural mechanisms that support memory formation.

5.2 PET Scans ​

Memory formation in the brain is a complex process that involves various neural systems and regions, and recent advances in neuroimaging techniques, particularly positron emission tomography (PET) scans, have significantly enhanced our understanding of these mechanisms.

Human memory is not a singular function; rather, it comprises multiple systems with distinct characteristics and specializations that are executed in the brain. The cognitive neuroscience of memory aims to elucidate how memories are encoded, stored, and retrieved across these systems. Functional neuroimaging techniques like PET provide the capability to observe the brain regions engaged in memory functions directly. PET, as a molecular imaging tool, allows for the investigation of the distribution and binding of radiochemicals to biologically relevant molecules, offering insights into the brain's biochemistry and metabolism during memory processes[35].

In terms of memory formation, specific brain regions play critical roles. The parahippocampal cortex (PHC) is essential for the formation of memories related to scenes. Research indicates that activation in the PHC can be monitored in real-time, and scene presentations can be triggered based on whether individuals are in a "good" or "bad" brain state for learning. This approach has demonstrated that subsequent recognition memory is more accurate for scenes presented during "good" brain states[36]. This suggests that the brain's state at the time of learning significantly influences memory formation and retention.

Moreover, neuroimaging studies have revealed that encoding and retrieval processes in memory involve specific brain regions that can be activated differently depending on the modality of the information being remembered. For instance, a PET study indicated that transperceptual encoding processes activate regions such as the right medial temporal lobe and the superior prefrontal cortex, highlighting that some memory processes operate beyond mere perceptual modalities[37].

The frontal lobes also contribute significantly to memory processing. Insights from functional neuroimaging have shown that different areas of the frontal cortex, such as the ventrolateral and dorsolateral regions, are activated during various memory stages, including working memory and episodic memory retrieval. These activations are linked to processes such as updating and maintaining information, as well as the selection and manipulation of that information[38].

Furthermore, the development of memory systems in the brain is an ongoing area of research. Neuroimaging studies suggest that memory development correlates with the maturation of the prefrontal cortex and the medial temporal lobes, which are crucial for memory strategy use and memory content representation, respectively[39].

In summary, memory formation involves intricate interactions between various brain regions, including the parahippocampal cortex and the frontal lobes, which are elucidated through advanced neuroimaging techniques like PET scans. These tools allow researchers to visualize and understand the neural correlates of memory processes, thereby enhancing our comprehension of how memories are formed, stored, and retrieved in the human brain.

5.3 Electrophysiological Techniques ​

Memory formation in the brain is a complex process that involves various cellular and molecular mechanisms. It is primarily associated with synaptic plasticity, particularly long-term potentiation (LTP), which is a long-lasting increase in synaptic efficacy following high-frequency stimulation of afferent fibers. This phenomenon is thought to be one of the key mechanisms underlying learning and memory, although empirical evidence linking LTP directly to memory storage remains limited [40].

The process of memory formation begins with the encoding of new information, which involves the activation of specific neuronal circuits. During this phase, synaptic connections between neurons are strengthened through various mechanisms, including the release of neurotransmitters and the activation of signaling pathways that promote synaptic changes [41]. For instance, brain-derived neurotrophic factor (BDNF) plays a crucial role in facilitating these synaptic changes during LTP by activating key signaling pathways, such as MAPK/ERK and PI3K/Akt [41].

Following encoding, memories undergo consolidation, which is a process that stabilizes and integrates newly formed memories into existing neural networks. This phase is often associated with sleep, during which the brain replays and reorganizes memories, enhancing their storage in long-term memory. Research suggests that sleep contributes to memory consolidation through mechanisms such as synaptic down-selection and the transfer of information from the hippocampus to neocortical areas [42].

Moreover, epigenetic mechanisms also play a vital role in memory formation. These mechanisms involve changes in gene expression without altering the DNA sequence itself, often mediated by histone modifications and DNA methylation. Recent studies have highlighted the dynamic nature of epigenetic regulation during memory formation, indicating that these processes are crucial for the transcriptional changes necessary for long-term memory [43].

The hippocampus, a critical brain region for memory processing, is particularly involved in the formation and consolidation of episodic memories. It houses specialized neurons that respond to specific stimuli, facilitating the encoding of the 'what' and 'where' components of memories [44]. The integration of information in the hippocampus relies on the coordinated activity of different neuronal populations, which are essential for forming coherent memory representations [44].

Overall, memory formation is a multifaceted process that encompasses the interplay of synaptic plasticity, molecular signaling, epigenetic regulation, and the dynamic reorganization of neuronal circuits. Advances in neuroimaging and electrophysiological techniques continue to enhance our understanding of these complex mechanisms, providing insights into how memories are formed, stored, and retrieved in the brain [4][26].

6 Implications for Memory Disorders ​

6.1 Alzheimer's Disease ​

Memory formation in the brain is a complex process that involves multiple neurobiological mechanisms, including synaptic plasticity, epigenetic modifications, and the interactions between various neural circuits. Central to this process is the role of specific brain regions, particularly the hippocampus and entorhinal cortex, which are crucial for episodic memory. Research indicates that memory formation requires alterations in synaptic efficacy, which are influenced by both pre- and postsynaptic changes in neural transmission and morphology. The Eph receptors and their cognate ephrin ligands have been identified as key players in these processes, regulating neurotransmitter release and dendritic spine morphology, which are vital for memory consolidation [45].

Epigenetic mechanisms, such as DNA methylation and histone modifications, have emerged as critical regulators of gene expression involved in memory formation. These mechanisms are influenced by neuronal activity and play a significant role in synaptic plasticity. Dysregulation of these epigenetic processes has been linked to cognitive decline and memory impairment, particularly in neurodegenerative disorders like Alzheimer's disease [46].

In Alzheimer's disease, memory impairment is one of the earliest and most prominent symptoms. The disease is characterized by the accumulation of amyloid-beta plaques and neurofibrillary tangles, which disrupt synaptic function and lead to cognitive deficits [47]. The memory and cognitive deficits observed in Alzheimer's are believed to result primarily from synaptic dysfunction, which can be exacerbated by environmental factors that influence gene expression [46].

The pathophysiology of Alzheimer's disease highlights the importance of the neuroimmune axis, where interactions between the nervous and immune systems contribute to cognitive dysfunction. Autoimmune responses may further complicate the disease process, suggesting that therapies targeting immune system interactions could be beneficial [48].

Recent studies have suggested that enhancing synaptic function through epigenetic agents or environmental enrichment may improve memory and cognitive function in Alzheimer's patients. This approach focuses on restoring the balance of epigenetic modifications to promote synaptic plasticity and memory retention [47]. Additionally, neurotrophins such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are implicated in the maintenance of synaptic integrity and have been shown to be affected early in Alzheimer's disease, contributing to the cascade of events leading to dementia [49].

In conclusion, memory formation in the brain involves a dynamic interplay of synaptic changes, epigenetic regulation, and the integrity of specific neural circuits. In the context of Alzheimer's disease, these processes become disrupted, leading to significant memory impairment and cognitive decline. Understanding these mechanisms offers potential avenues for therapeutic interventions aimed at enhancing memory function and addressing the underlying pathophysiology of neurodegenerative diseases.

6.2 PTSD ​

Memory formation is a complex process involving multiple brain regions and molecular mechanisms. It encompasses the encoding, consolidation, retrieval, and extinction of memories, which are essential for learning and adapting to experiences. The hippocampus, amygdala, and prefrontal cortex (PFC) are particularly crucial in these processes, especially concerning emotionally charged memories, such as those related to traumatic experiences.

During memory formation, neurons in the hippocampus undergo synaptic plasticity, where the strength of connections between neurons is enhanced. This process is influenced by various proteins regulated through epigenetic mechanisms, including DNA methylation and histone modifications, which can lead to long-lasting changes in cellular function. Neurosteroids have also been implicated in modulating these processes, suggesting that their involvement in epigenetic control may have therapeutic potential for memory-related disorders [50].

The role of stress in memory formation is significant, particularly in the context of post-traumatic stress disorder (PTSD). Acute stress can enhance the consolidation of aversive memories, which may be beneficial for survival but can also lead to maladaptive outcomes, such as PTSD. Research indicates that stress hormones affect attentional and mnemonic processes during memory formation, leading to heightened recall of traumatic events [51]. This stress response can result in persistent and intrusive memories, characteristic of PTSD, where individuals may relive their trauma through involuntary recollections [52].

Epigenetic mechanisms play a pivotal role in the formation and maintenance of fear memories associated with PTSD. These mechanisms can influence gene expression related to memory processes, thereby supporting the persistence of fear associations. Targeting these epigenetic changes may offer new avenues for treatment, aiming to reduce the formation of fear memories or enhance their extinction [53].

The neural correlates of memory retrieval in PTSD also differ from those in non-affected individuals. Studies utilizing functional neuroimaging have shown that individuals with PTSD exhibit increased activation of the amygdala and decreased engagement of the PFC when retrieving negative memories. This imbalance may lead to difficulties in controlling emotional responses to traumatic memories, contributing to the symptoms of PTSD [54].

Moreover, the cognitive abnormalities observed in PTSD patients include deficits in declarative memory functioning, which are linked to the dysregulation of the hippocampus and PFC. These abnormalities may manifest as verbal memory deficits, overgeneralized memories, and avoidance of trauma-related recollections [55]. Such disturbances highlight the intricate relationship between memory processes and the psychological impact of trauma.

In conclusion, memory formation in the brain is a dynamic process influenced by various neurobiological and epigenetic factors. The interplay between stress, memory encoding, and retrieval mechanisms elucidates the complexities of PTSD, where alterations in memory processes contribute to the disorder's symptoms. Understanding these mechanisms can pave the way for innovative therapeutic strategies aimed at alleviating the burdens of memory-related disorders, particularly PTSD.

6.3 Other Memory-Related Conditions ​

Memory formation in the brain is a complex process that involves multiple molecular and cellular mechanisms. The brain is equipped with both mechanisms that facilitate memory formation and those that suppress it, ensuring an efficient memory management system. This duality is essential, as individuals are constantly exposed to vast amounts of information, most of which becomes irrelevant over time. The brain utilizes various processes to select critical information for storage while suppressing or forgetting the irrelevant (Noyes & Davis, 2024) [3].

The formation of long-term memories is closely associated with alterations in synaptic efficacy, which result from changes in neural transmission and the morphology of synapses. Eph receptors and their cognate ephrin ligands play a significant role in these processes by regulating presynaptic transmitter release, postsynaptic glutamate receptor conductance, and dendritic spine morphogenesis. These proteins are crucial for memory formation across different organisms and are implicated in various brain disorders, including Alzheimer's disease and anxiety, suggesting that they may serve as therapeutic targets (Dines & Lamprecht, 2016) [45].

Additionally, microglia have recently been recognized for their role in memory formation through the regulation of synaptic architecture. They facilitate synaptic formation by clearing extracellular matrix proteins, thereby allowing for dynamic remodeling of synaptic connections (Zaki & Cai, 2020) [10]. This remodeling is essential for the encoding and retrieval of memories, as it underpins the synaptic plasticity required for learning.

Memory persistence, while vital for survival, can lead to maladaptive memories that contribute to psychiatric conditions such as post-traumatic stress disorder and substance dependence. The neurobiological mechanisms underlying memory persistence and inhibition are critical for understanding these disorders, as they reveal how memories can be altered or suppressed (Merlo et al., 2024) [56].

Epigenetic mechanisms also play a significant role in memory formation. They involve changes in gene expression that occur in response to external stimuli, influencing synaptic plasticity and memory development. Dysregulation of these epigenetic processes can lead to cognitive and memory impairments associated with neurodegenerative diseases such as Alzheimer's and Huntington's disease (Rosales-Reynoso et al., 2016) [57].

The cholinergic system is another critical player in memory formation. Disruption of cholinergic pathways is a hallmark of memory-related disorders, and studies have shown that cholinergic blockade can impair memory by affecting theta oscillations in the hippocampus, which are essential for encoding memories (Gedankien et al., 2023) [58].

Overall, the mechanisms of memory formation are multifaceted, involving intricate interactions between various cellular and molecular components. Understanding these processes is essential for developing therapeutic strategies to address memory-related disorders and conditions. As research continues to unveil the complexities of memory mechanisms, it offers hope for interventions that could ameliorate the impacts of memory impairments on individuals' lives.

3 Conclusion ​

The investigation into memory formation has yielded significant insights into the intricate mechanisms underlying this fundamental cognitive process. Key findings indicate that memory can be categorized into declarative and non-declarative types, each supported by distinct neural structures and mechanisms. The hippocampus emerges as a central player in declarative memory, while the amygdala significantly influences emotional memory retention. Advances in neuroimaging techniques have provided a deeper understanding of the neural circuitry involved in memory, revealing how different brain regions interact during the encoding and retrieval processes. Additionally, molecular and cellular mechanisms, particularly synaptic plasticity, neurotransmitter activity, and hormonal influences, play critical roles in memory formation. However, the implications of these findings extend beyond academic inquiry; they hold potential for therapeutic interventions in memory-related disorders such as Alzheimer's disease and PTSD. Future research directions should focus on elucidating the complex interactions between different memory systems, the role of epigenetic modifications, and the potential for developing targeted treatments that can enhance memory function and address cognitive impairments. By continuing to unravel the complexities of memory formation, we move closer to improving interventions for those affected by memory disorders and enhancing our understanding of the remarkable capabilities of the human brain.

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