Dementia profoundly influences brain activity during rest by disrupting the normal patterns of functional connectivity and neural dynamics that characterize a healthy brain. Resting-state brain activity refers to the spontaneous neural activity occurring when a person is not engaged in any specific task, often studied using resting-state functional magnetic resonance imaging (rs-fMRI) or electroencephalography (EEG). In dementia, especially Alzheimer’s disease (AD) and related disorders, these resting-state networks (RSNs) show altered connectivity, reduced synchrony, and abnormal oscillatory patterns that reflect underlying neurodegeneration and cognitive decline.
One of the most studied resting-state networks affected by dementia is the default mode network (DMN). The DMN includes brain regions such as the posterior cingulate cortex, medial prefrontal cortex, inferior parietal lobule, and the medial temporal lobe (MTL), including the hippocampus. In healthy individuals, the DMN is more active during rest and deactivates during attention-demanding tasks. This network is crucial for episodic memory, self-referential thought, and internal mentation. In dementia, particularly AD, the DMN shows disrupted functional connectivity both within itself and with other networks, such as the dorsal attention network (DAN) and executive attention networks. These disruptions manifest as reduced integration between the hippocampus and DMN regions, impaired anticorrelation between DMN and attention networks, and altered spontaneous fluctuations of neural activity during rest[1][5].
Functional MRI studies reveal that in individuals at risk for AD or with mild cognitive impairment (MCI), there is a selective alteration in resting-state networks. The connectivity between the hippocampus and DMN weakens, which correlates with memory deficits and early neurodegeneration. Additionally, the executive attention network, which normally interacts in an anticorrelated manner with the DMN, shows functional disconnectivity, aligning with observed attentional impairments in dementia[1]. These changes suggest that dementia disrupts the brain’s intrinsic organization, impairing the balance and coordination between networks that support cognition.
Beyond static connectivity, dynamic functional connectivity (dFC) studies show that dementia affects the stability and transitions between different brain states during rest. Early in the disease, such as in subjective cognitive decline (SCD), abnormalities appear as altered transition probabilities between brain states. As dementia progresses to MCI and AD, there is a collapse in the intrinsic stability of key cognitive network states, with reduced dwell time and occurrence rates of states involving the DMN and visual networks. This instability reflects a loss of the brain’s ability to maintain coherent network activity over time, which is critical for cognitive function[2].
Electrophysiological studies using resting-state EEG complement fMRI findings by showing spectral slowing and reduced neural synchrony in dementia. Patients with AD exhibit decreased alpha and beta power and increased delta and theta power, indicating a shift toward slower brain rhythms. These changes are widespread and not limited to the DMN, suggesting global brain dysfunction. Reduced synchrony between brain regions, especially in the alpha band, correlates with cognitive impairment and structural brain atrophy[3][9].
Animal studies using resting-state fMRI in mouse models of Alzheimer’s disease provide additional insights. These studies show that mechanical stimulation techniques can modulate resting-state functional connectivity in limbic and subcortical regions involved in memory and emotional regulation. Although these findings cannot be directly translated to humans, they highlight the plasticity of resting-state networks and their potential as targets for therapeutic intervention in dementia[4].
The interaction between large-scale networks during rest is also altered in dementia. Normally, the DMN and DAN exhibit an on/off relationship, where activation of one suppresses the other. This balance supports switching between internal thought and external attention. In dementia, this anticorrelation weakens, leading to a “functional imbalance” that may underlie cognitive decline. Studies using resting-state fMRI in cohorts with varying amyloid burden show that the strength of DMN-DAN anticorrelation tracks with Alzheimer’s pathology and cognitive performance, suggesting that resting-state network interactions could serve as biomarkers for disease progression[5].
In dementia with Lewy bodies (DLB), another common form of dementia, resting-state functional connectivity abnormalities also involve the DMN and visual networks. These disruptions correlate with cognitive impairment and may differ in pattern from those seen in AD, reflecting disease-specific network dysfunction[6].
Longitudinal studies tracking functional connectivity changes during rest and task states emphasize that alterations in episodic memory networks occur early and evolve with disease progression. These changes highlight the dynamic nature of resting-state brain activity in dementia and its close relationship with cognitive decline[7].
In summary, dementia influences brain activity during rest by disrupting the normal functional connectivity and dynamic stability of key brain networks, especially the default mode network and its interactions with attention and executive networks. These alterations reflect underlying neurodegeneration, contribute to cognitive symptoms, and offer potential targets for diagnosis and intervention. The evidence comes from multiple modalities including rs-fMRI, EEG, and animal models, providing a comprehensive picture of how dementia reshapes the brain’s intrinsic activity patterns.
Sources:
[1] Proceedings of the National Academy of Sciences (PNAS), 2007
[2] PMC – Dynamic functional connectivity and transcriptomic signatures, 2025
[3] Science Advances, 2025
[4] STORZ Medical Blog, 2025
[5] Medical Xpress, 2025
[6] Frontiers in Aging Neuroscience, 2025
[7] Nature Scientific Reports, 2025
[9] PMC – Brain Topology Disruption in Early-Onset Dementia
