Dissociable Impacts of Alzheimer's Disease and Aging on Brain Network
Amidst the intricate tapestry of the human brain, Alzheimer's disease (AD) and aging weave distinct patterns of disruption, altering the delicate balance of interconnected networks. This article delves into the dissociable impacts of AD and aging on brain network organization, illuminating the neuroanatomical underpinnings of cognitive decline.
DR T S DIDWAL MD
11/22/20233 min read
AD patients exhibit less segregated resting-state brain networks compared with healthy control participants.
Brain system segregation also changes over the course of healthy adult ageing in the absence of AD: Brain system segregation declines with increasing adult age.
The study found that AD and aging have dissociable impacts on the brain's functional connectome.
AD-associated brain network alterations were widespread and involved systems that subserve not only higher-order cognitive operations but also sensory and motor operations.
AD-related network alterations were independent of amyloid pathology.
Alzheimer's disease (AD), a neurodegenerative disorder characterized by progressive cognitive decline, is the most common cause of dementia worldwide. Aging, the natural process of biological decline associated with increasing chronological age is the most significant risk factor for AD. Both AD and aging are associated with changes in the organization of large-scale brain networks, the intricate web of connections between different brain regions. Understanding how these network alterations differ between AD and normal aging is crucial for early diagnosis, effective treatment, and ultimately, prevention.
The Brain's Functional Connectome: A Symphony of Networks
The brain's functional connectome, the blueprint of its interconnectedness, is a dynamic and complex system that orchestrates our thoughts, memories, and actions. It comprises a mosaic of specialized brain networks, each subserving specific cognitive functions. These networks are not isolated entities but rather interact seamlessly through a vast network of connections.
AD and Aging: Disparate Impacts on Brain Network Segregation
Brain system segregation, a measure of the division of the brain into distinct functional modules, is a critical aspect of network organization. It facilitates efficient information processing and enables the specialized functioning of different brain regions. Both AD and aging have been shown to disrupt brain system segregation but in distinct ways.
AD patients exhibit reduced brain system segregation compared to healthy individuals. This suggests a breakdown of the modular organization of the brain, leading to less efficient communication between different brain regions. This disruption is likely a contributing factor to the cognitive impairments observed in AD.
Aging, on the other hand, is associated with a more subtle decline in brain system segregation. This age-related decline is thought to reflect the gradual accumulation of cellular and molecular damage throughout the brain. While less pronounced than in AD, this decline may also contribute to subtle cognitive changes observed in older adults.
Distinguishing AD from Aging: A Tale of Two Networks
The impact of AD and aging on brain network organization is not uniform across all brain systems. AD-related network alterations are most prominent in association systems, and responsible for higher-order cognitive functions such as memory and executive function. In contrast, aging-related network alterations are more evident in sensory-motor systems, involved in processing sensory information and controlling movement.
Furthermore, AD and aging exhibit distinct patterns of network interactions. AD-related alterations are more pronounced among cross-system interactions, the connections between different brain systems. Aging-related alterations, on the other hand, are more evident within-system interactions, the connections within a particular brain system.
Unravelling the Mystery: The Role of Amyloid Pathology
Amyloid plaques, abnormal clumps of proteins that accumulate in the brain, are a hallmark of AD pathology. Their presence is thought to contribute to the neurodegeneration and cognitive decline observed in AD. However, the relationship between amyloid pathology and brain network alterations is complex.
Recent studies have shown that amyloid pathology is not directly associated with brain system segregation. This suggests that the network alterations observed in AD are not solely driven by amyloid accumulation but may involve other pathological mechanisms.
Towards a Comprehensive Understanding of AD and Aging
The intricate relationship between AD and aging on brain network organization is a complex puzzle with many missing pieces. While significant progress has been made in understanding the dissociable impacts of AD and aging on network alterations, further research is needed to fully unravel the underlying mechanisms and their implications for diagnosis, treatment, and prevention.
Future research should focus on elucidating the specific network interactions that are disrupted in AD and aging, investigating the role of additional pathological factors beyond amyloid, and exploring the potential of brain network measures as biomarkers for early detection and disease progression monitoring.
Conclusion: A New Frontier in Brain Health
By understanding the intricate interplay between AD and aging on brain network organization, we can advance our understanding of the underlying mechanisms of neurodegeneration and cognitive decline. This knowledge has the potential to revolutionize the diagnosis, treatment, and prevention of AD, improving the quality of life for millions of individuals worldwide and alleviating the burden on families and caregivers.
Journal Reference:
Ziwei Zhang, Micaela Y. Chan, Liang Han, Claudia A. Carreno, Ezra Winter-Nelson, Gagan S. Wig. Dissociable Effects of Alzheimer's Disease-Related Cognitive Dysfunction and Aging on Functional Brain Network Segregation. The Journal of Neuroscience, 2023; 43 (46): 7879 DOI: 10.1523/JNEUROSCI.0579-23.2023
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