Biology subjects

Weinstein, A. M.

Publications and source records attributed to Weinstein, A. M..

4 recordsLinked to original sources

bioRxiv2026

Locomotor savings relies on attentional control of walking in older, but not younger adults

The ability to recall learned movements and rapidly adapt to environmental changes, known as locomotor savings, is crucial for mobility in community-dwelling older adults. However, the influence of aging on locomotor savings and the underlying mechanisms remains poorly understood. Attentional compensation is a particularly relevant mechanism because the control of automatic motor behaviors like walking tend to recruit more attentional/executive resources with aging. We hypothesize that locomotor savings is diminished with age and relies on attentional rather than automatic control of walking. To test this, we compared savings of a novel walking pattern learned on a split-belt treadmill, where each leg moves at a different speed, across multiple days in 21 older and 21 younger adults. Attentional control of walking was assessed by overground dual-task walking while prefrontal cortex (PFC) activity was recorded using functional near-infrared spectroscopy (fNIRS). We found that older adults exhibited less locomotor savings than younger adults after practice. Older adults also relied more on attentional resources during dual-task walking. Importantly, greater locomotor savings was associated with higher attentional control of walking in older adults, suggesting that the use of attentional resources during challenging walking facilitates the recall of previously learned movements. These results indicate that cognitive compensation strategies utilizing attentional resources are important neural mechanisms modulating locomotor savings. Understanding the role of cognitive compensation in locomotor savings may inform rehabilitation design to enhance mobility in older adults ensuring movement corrections practiced in clinical settings are saved for long-term benefit in daily life.

neuroscience↗

bioRxiv2023

Novel automaticity index characterizing dual task walking reveals a cognitive ability-related decline in gait automaticity.

Gait automaticity refers to the ability to walk with minimal recruitment of attentional networks typically mediated through the prefrontal cortex (PFC). Reduced gait automaticity is common with aging, contributing to an increased risk of falls and reduced quality of life. A common assessment of gait automaticity involves examining PFC activation using near-infrared spectroscopy (fNIRS) during dual-task (DT) paradigms, such as walking while performing a cognitive task. However, neither PFC activity nor task performance in isolation measures automaticity accurately. For example, greater PFC activation could be interpreted as worse gait automaticity when accompanied by poorer DT performance, but when accompanied by better DT performance, it could be seen as successful compensation. Thus, there is a need to incorporate behavioral performance and PFC measurements for a more comprehensive evaluation of gait automaticity. To address this need, we propose a novel automaticity index as an analytical approach that combines changes in PFC activity with changes in DT performance to quantify gait automaticity. We validated the index in 173 participants ([≥]65 y/o) who completed DTs with two levels of difficulty while PFC activation was recorded with fNIRS. The two DTs consisted of reciting every other letter of the alphabet while walking over either an even or uneven surface. We found that as DT difficulty increases, more participants showed the anticipated decrease in automaticity as measured by the novel index compared to PFC activation. Furthermore, when comparing across individuals, lower cognitive function related to worse automaticity index, but not PFC activation or DT performance. In sum, the proposed index better quantified the differences in automaticity between tasks and individuals by providing a unified measure of gait automaticity that includes both brain activation and performance. This new approach opens exciting possibilities to assess participant-specific deficits and compare rehabilitation outcomes from gait automaticity interventions.

neuroscience↗

bioRxiv2022

Critical pollination chemistry: Specific sesquiterpene floral volatiles in carrot inhibit honey bee feeding.

O_LIAlthough many plant species are reliant on insect pollination, agricultural plant breeding programs have primarily focused on traits that appeal to growers and consumers, rather than on floral traits that enhance pollinator attraction. In some vegetable seed production systems, this has led to declining pollinator attraction and poor seed yields. C_LIO_LIWe predicted that low-yielding crop varieties would be less attractive to pollinators due to deficiencies in nectar rewards or volatile floral attractants. To test our prediction, we used a chemical phenotyping approach to examine how floral chemical traits of five carrot lines affect honey bee visitation. C_LIO_LIIn bioassays, honey bees avoided feeders containing nectar from all carrot lines indicating a general non-attractant effect. Certain compounds in carrot flowers and nectar not only failed to elicit attraction but functioned as repellents, including the sesquiterpenes -selinene and {beta}-selinene. Others enhanced attraction, e.g. {beta}-ocimene. C_LIO_LIThe repellent sesquiterpenes have previously been implicated in plant defense suggesting a fine balance between pollination and plant protection, which when disrupted in artificial selection in plant breeding programs can impact the crop yield. These new insights highlight the importance of bioactive compounds in attracting pollinators toward floral resources in both ecological and agricultural settings. C_LI

plant biology↗

bioRxiv2022

A mitochondrial blood-based patient stratification candidate biomarker for Parkinson's disease

Parkinsons disease (PD) is the most common neurodegenerative movement disorder and neuroprotective interventions remain elusive. High throughput biomarkers aimed to stratify patients based on shared etiology is one critical path to the success of disease-modifying therapies in clinical trials. Mitochondrial dysfunction plays a prominent role in the pathogenesis of PD. Previously, we found brain region-specific mitochondrial DNA (mtDNA) damage accumulation in neuronal and in vivo PD models, as well as human PD postmortem brain tissue. In this study, to investigate mtDNA damage as a potential blood biomarker for PD, we describe a novel Mito DNADX assay that allows for the accurate real-time quantification of mtDNA damage in a 96-well platform, compatible with assessing large cohorts of patient samples. We found that levels of mtDNA damage were increased in blood derived from early-stage idiopathic PD patients or those harboring the pathogenic LRRK2 G2019S mutation compared to age-matched healthy controls. Given that increased mtDNA damage was also found in non-manifesting LRRK2 mutation carriers, mtDNA damage may begin to accumulate prior to a clinical PD diagnosis. LRRK2 kinase inhibition mitigated mtDNA damage in idiopathic PD models and patient-derived cells. The latter observations further substantiate a mechanistic role for wild-type LRRK2 kinase activity in idiopathic PD and support mtDNA damage reversal as a suitable approach to slow PD-related pathology. In light of recent advances in the field of precision medicine, the analysis of mtDNA damage as a blood-based patient stratification biomarker should be included in future clinical trials. One Sentence SummaryBlood test identifies Parkinsons patients most likely to respond to mitochondria-targeted therapeutics facilitating a precision medicine approach.

neuroscience↗