Structural Compensation and Participatory Approaches: A Way to Improve Access to Health Care for Undocumented Immigrants? A Scoping Review.

Cognition is a process in which the human brain takes in external information, processes it, transforms it into internal psychological operations, and acquires knowledge or applies that knowledge (Miller et al., 2024). It encompasses memory, language, visual-spatial skills, executive function, calculation, comprehension, and judgment (Wang et al., 2024). Cognitive impairment refers to the deterioration of one or more of the aforementioned cognitive functions, which impacts an individual’s daily and social capabilities (Lee and Jung, 2024; You et al., 2024). With the increasingly evident trend of population aging, the issue of cognitive impairment has attracted widespread attention (El Husseini et al., 2023). The primary pathological mechanism of cognitive impairment is closely related to the dysfunction of neural circuits and cell damage in specific brain regions. Pathological processes such as neuroinflammation, abnormal protein aggregation (e.g., amyloid-β [Aβ] and tau protein aggregation), and neurotransmitter imbalance selectively target key circuit nodes (e.g., the hippocampus and prefrontal cortex), resulting in decreased information transmission efficiency and disrupted network connectivity, which ultimately manifests as a decline in specific cognitive functions (Mok et al., 2024). Recent studies have revealed that several brain regions, such as the medial temporal lobe, prefrontal cortex (Miller and Cohen, 2001; Friedman and Robbins, 2022), parietal cortex (Culham and Kanwisher, 2001; Cabeza et al., 2012; Freedman and Ibos, 2018), amygdala (Gallagher and Chiba, 1996; LeDoux, 2000; Meisner et al., 2022), basal nucleus of Meynert (Chen et al., 2023), and striatum (Chersi and Burgess, 2015), are confirmed to be involved in cognitive function. The medial temporal memory system is composed of the hippocampus and adjacent related cortices, including the entorhinal cortex, perirhinal cortex, and parahippocampal cortex, which play a crucial role in long-term memory, specifically declarative memory (Squire and Zola-Morgan, 1991; Clark, 2018). As a key hub of the limbic system, the hippocampus has become the focus of research on cognitive decline due to its central role in memory encoding, spatial navigation, and situational integration. Over the past two decades, advancements in optogenetics, single-cell sequencing, and calcium imaging have gradually revealed the specific contributions of heterogeneous cell populations in the hippocampus, such as CA1–CA3 pyramidal cells, dentate gyrus (DG) granule cells, and interneurons, to the maintenance of cognitive function. An early study primarily focused on the relationship between hippocampal atrophy and cognitive impairment-related diseases (Jia et al., 2025). However, recent findings indicate that the process of cognitive decline often precedes obvious structural changes, suggesting that microscopic cellular dysfunction may serve as a more sensitive warning indicator. For example, reduced dendritic spine density in pyramidal cells in the CA1 region disrupts the neural representation of spatial memory, while neurogenic defects in granule cells in the DG are directly associated with reduced pattern separation ability. Notably, glial cells indirectly exacerbate neuronal network imbalance by altering the local microenvironment, such as through glutamate reuptake disorders in astrocytes and abnormal synaptic pruning in microglia (Lee et al., 2021). These findings challenge the limitations of the traditional “neuron-centric theory” and emphasize the dynamic balance of cell interaction networks in the maintenance of cognition. The causes of cognitive impairment are multifactorial, with cerebrovascular events (e.g., cerebral hemorrhage and infarction) and neurodegenerative conditions serving as core drivers. Inflammation, metabolic abnormalities, and psychological states act synergistically to accelerate the disease course. Clinical evaluation requires the integration of imaging, biomarkers, and neuropsychological testing. However, a central yet not fully answered scientific question remains: why do vascular events, neurodegenerative lesions, or metabolic abnormalities trigger the dysfunction of critical cells (e.g., neurons and neural stem/progenitor cells) in specific brain regions (e.g., the hippocampus) and ultimately lead to clinical symptoms such as memory loss and executive dysfunction? Furthermore, a previous study has shown that neurogenesis in the DG of the hippocampus, a rare process involving the continuous generation of new neurons in the adult brain, plays a key role in learning, memory (especially pattern separation), and emotion regulation (Qin et al., 2022). A decline in or impairment of nerve regeneration capacity is an important early pathological feature of various cognitive disorders (e.g., Alzheimer’s disease [AD] and vascular dementia). However, the changes that occur at different stages of the disease, the specific mechanisms of damage (e.g., micr