Biology subjects

Freedberg, M. V.

Publications and source records attributed to Freedberg, M. V..

6 recordsLinked to original sources

bioRxiv2026

Non-invasive Neuromodulation Targeting Approach by Mapping Stimulations and Lesions That Modify Visual Memory

Therapeutic brain stimulation is believed to target specific networks, but targeting approaches for memory remain debated. For other symptoms, neuromodulation targets have been localized by mapping connectivity of lesions and stimulation sites to specific symptoms. This approach has yielded networks for global memory, but it remains unclear whether it applies to specific types of memory. Here, we mapped connectivity of stimulation sites, lesions, and atrophy patterns associated with different memory types. We included 544 individuals across three datasets: transcranial magnetic stimulation (N=262), penetrating head trauma (N=169), and ischemic stroke (N=113). We identified a network preferentially connected to lesions and stimulation sites specifically associated with changes in visual memory. Of note, the direction of this effect was inverted depending on whether lesions or stimulation occurred at younger age or an older age, consistent with prior results. This age effect was replicated in an independent dataset of patients with preclinical Alzheimers disease (N=1240). To examine neuromodulation targets, we computed electrical field models for potential TMS sites that overlap with the networks derived from each stimulation or lesion dataset; the resulting targets intersected with established targets that demonstrated efficacy for treating memory impairment - precuneus, cortical-hippocampal network, and dorsolateral prefrontal cortex - with peak intersection at medial posterior parietal lobe, angular gyrus, and left anterior middle frontal gyrus, respectively. Future head-to-head clinical trials are needed to systematically compare these proposed neuromodulation targets against each other. One Sentence SummaryNeuromodulation targets for visual memory diverge by age at the time of injury or stimulation.

neuroscience↗

bioRxiv2025

Asymmetric increase in episodic and procedural memory interference in older adults

In younger adults, newly formed procedural memories are weakened by the subsequent formation of episodic memories (E[->]P interference) and vice versa (P[->]E interference; "cross-memory interference"). Older adults experience significant decline in episodic memory but maintain relatively intact procedural memory. This asymmetric decline in memory may also cause an asymmetric change in cross-memory interference compared to younger adults. For example, older adults may experience a significant increase in one type of cross-memory interference while leaving the other unchanged. Additionally, decline in episodic memory may cause E[->]P interference to either increase or decrease depending on how the episodic and procedural memory systems interact. However, no study to our knowledge has compared cross-memory interference between younger and older adults. We investigated cross-memory interference in younger and older adults by measuring E[->]P (Exp. 1) and P[->]E (Exp. 2) interference in 40 younger (18-40 years old) and 40 older ([≥] 55 years old) adults. Compared to younger adults, the results show that older adults experience significantly stronger E[->]P interference while P[->]E interference was statistically indistinguishable between groups. These results confirm that older adults experience an asymmetric increase in cross-memory interference and suggest that the increase in E[->]P interference is related to the asymmetric decline in episodic memory relative to procedural memory.

neuroscience↗

bioRxiv2024

Failure to reproduce the effect of procedural memory interference on wakeful consolidation of episodic memory in younger and older adults

Brown and Robertson (2007) revealed that skill learning interferes with the wakeful consolidation of episodic memories in young adults. This finding is commonly used as evidence that episodic and procedural memories should not be learned in close temporal proximity but has not been reproduced by an independent laboratory. Additionally, older adults experience episodic memory deficits, but it is unknown whether this group is also vulnerable to this type of interference. We aimed to reproduce Brown and Robertsons (2007) finding in younger adults, while also comparing the magnitude of interference between younger and older adults. Forty younger (18-40 years; n =20) and older adults ([≥]55 years; n = 20) visited the laboratory in the morning and acquired episodic memories (a list of words) immediately before a procedural finger-tapping (procedural) task. Half of all participants were exposed to a learnable sequential structure. In the afternoon of the same day, participants were asked to recall the episodic memories from the morning session. We found weak evidence of interference for both age groups and no statistical difference in interference between groups. Our results suggest that the interfering effects of these memory types may be negligible or overestimated, and that these memory types can be acquired together without interference.

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bioRxiv2024

Motor sequence learning-induced corticospinal plasticity is biased towards sensorimotor mu rhythm peak phases

Motor cortical (M1) transcranial magnetic stimulation (TMS) interventions increase corticospinal output and improve motor learning when delivered during sensorimotor mu rhythm trough but not peak phases, suggesting that the mechanisms supporting motor learning may be most active during mu trough phases. Based on these findings, we predicted that motor sequence learning-related corticospinal plasticity would be most evident when measured during mu trough phases. Healthy adults were assigned to either a sequence or no-sequence group. Participants in the sequence group practiced the implicit serial reaction time task (SRTT), which contained an embedded, repeating 12-item sequence. Participants in the no-sequence group practiced a version of the SRTT that contained no sequence. We measured mu phase-independent and mu phase-dependent MEP amplitudes using EEG-informed single-pulse TMS before, immediately after, and 30 minutes after the SRTT in both groups. All participants performed a retention test one hour after SRTT acquisition. In both groups, mu phase-independent MEP amplitudes increased following SRTT acquisition, but the pattern of mu phase-dependent MEP amplitude changes after SRTT acquisition differed between groups. Relative to the no-sequence group, the sequence group showed greater peak-specific MEP amplitude increases 30 minutes after SRTT acquisition. Further, the magnitude of these peak-specific MEP amplitude increases was negatively associated with the magnitude of sequence-specific learning. Contrary to our original hypothesis, results revealed that motor sequence-specific learning elicits peak-specific corticospinal plasticity. Findings provide first direct evidence for the presence of a mu phase-dependent motor learning mechanism in the human brain. New and NoteworthyRecent work suggests that motor learnings neural mechanisms may be most active during specific sensorimotor mu rhythm phases. If so, motor sequence learning-induced corticospinal plasticity should be more evident during some mu phases than others. Our results show that motor sequence-specific learning elicits corticospinal plasticity that is most prominent during mu peak phases. Further, this peak-specific plasticity correlates with learning. Findings establish the presence of a mu phase-dependent motor learning mechanism in the human brain.

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bioRxiv2022

Hippocampal and caudate network specificity is altered in older adults

The hippocampal and the caudate networks, defined by their intrinsic resting state functional connectivity (FC), exhibit strong network specificity. This is reflected as strong within-network and weak between-network FC, as well as their dissociable roles in cognition. Aging typically reduces the specificity of brain networks. However, whether the hippocampal and caudate networks show age-related decreases in network specificity is unclear. Further, whether any age-related decreases in network specificity are due to reduced within-network FC, increased between-network FC, or some combination of both, is also unclear. Using a large-scale fMRI data set acquired from healthy younger (n = 101, aged 18-40 years) and older (n = 101, 55-75 years) adults, networks centered on the left anterior hippocampus and the head of the right caudate nucleus were compared. These sub-regions were chosen based on their distinct contributions to cognition, their known interactions, and their susceptibility to age-related changes. A mixed effect model was used to identify brain regions where network specificity differed between groups. For younger adults, hippocampal network specificity was strong in the medial frontal gyrus (MFG), while caudate network specificity was strong in the basal nuclei. However, network specificity in these same regions was significantly reduced in older adults. Reduced specificity in each network was due to a weakening of within-network connectivity rather than an increase in between-network connectivity. These results indicate that hippocampal and caudate network specificity decreases with advancing age, raising the possibility that these reductions may contribute to age-related changes in memory. Impact StatementOlder adults represent an increasing proportion of the population, thus increasing the urgency for us to understand the neurological changes that contribute to age-related memory loss. Aging is associated with a loss of network specificity, reflected as reduced within-network, and increased between-network, connectivity. My work shows that this phenomenon is not restricted to the hippocampal and caudate networks, which are critical for learning facts and skills, respectively: Both networks decreased in network functional connectivity. These results raise the possibility that "blurring" between these networks relates to age-related memory loss, possibly as a compensatory mechanism to protect memory in old age.

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bioRxiv2019

Identifying site- and stimulation-specific TMS-evoked EEG potentials using a quantitative cosine similarity metric

The ability to interpret transcanial magnetic stimulation (TMS) evoked EEG potentials (TEPs) is limited by artifacts, such as auditory evoked responses produced by the TMS coil. TEPs generated from direct cortical stimulation should vary in spatial distribution with stimulation site and from responses to sham stimulation. Responses that do not show these effects are likely to be artifactual. In 20 healthy volunteers, we delivered active and sham TMS to right prefrontal, left primary motor, and left posterior parietal cortex and compared the waveform similarity of TEPs between stimulation sites and active and sham TMS with a cosine similarity-based analysis method. We looked for epochs after the stimulus when the spatial pattern of TMS-evoked activation had greater than random similarity between stimulation sites and sham vs. active TMS, indicating presence of a dominant artifact, such as the auditory brain response. We calculated and binarized the derivatives of the TEPs recorded from 30 EEG channels and calculated cosine similarity between conditions at each time point with millisecond resolution. Only TEP components occurring before approximately 80 ms differed across stimulation sites and between active and sham, indicating site and condition-specific responses. TEP components before about 80 ms can be safely interpreted as stimulation location-specific responses to TMS, but components beyond this latency should be interpreted with caution due to high similarity in their spatial distribution.

neuroscience↗