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Temporal pole initiation of neuronal avalanches is associated with episodic Memory performance in Mild Cognitive Impairment

Gallo, E.; Demuru, M.; De Luca, M.; Troisi Lopez, E.; Granata, C.; Nappo, R.; Corsi, M.-C.; Sorrentino, G.; Depannemaecker, D.; Angiolelli, M.; Sorrentino, P.

2026-08-02 neurology
10.64898/2026.07.30.26359001 medRxiv
Show abstract

Episodic-memory impairment is a defining feature of Mild cognitive impairment (MCI), yet the large-scale neural processes through which medial temporal pathology translates into poor cognitive performance remain unclear. Fast brain activity can be organized into transient, aperiodic bursts--neuronal avalanches--that propagate from hippocampal and adjacent temporal regions across distributed brain networks, potentially indexing interactions relevant to memory. We therefore hypothesized that episodic-memory impairment in MCI reflects an altered ability of the temporal pole to initiate these activity cascades. We analyzed resting-state, source-reconstructed MEG recordings from 29 individuals with MCI and 32 healthy controls (HC). Large-scale dynamics were described in terms of neuronal avalanches, and we quantified each temporal-pole region 's propensity to act as an ''avalanche starter''--that is, to be the first region to become active. We then related this measure to episodic-memory performance and hippocampal volume. Although temporal-pole starter frequency did not differ between groups, its relationship with memory performance was reversed. Greater avalanche initiation from the left temporal pole was associated with poorer memory performance in MCI, as measured by the delayed free recall in the Free and Cued Selective Reminding Test. The same relationship was positive in HC. Within the MCI group, greater left-temporal-pole starter frequency was also associated with hippocampal atrophy. These findings suggest that MCI involves a qualitative reorganization of temporal-pole initiated dynamics rather than a simple change in their frequency. This framework links local structural vulnerability to altered whole-brain dynamics and episodic-memory impairment.

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