Margaret Fahnestock | McMaster University (original) (raw)
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Papers by Margaret Fahnestock
International Journal of Molecular Sciences, Mar 9, 2017
Journal of comparative neurology, Jul 19, 2011
Journal of Neurosurgery, Nov 1, 2008
Progress in Neurobiology, May 1, 2004
Frontiers in Neuroscience, Feb 22, 2019
Neurobiology of Aging, Aug 1, 2015
Molecular Brain Research, Nov 1, 1996
Brain Research, Nov 1, 1993
Alzheimers & Dementia, Jul 1, 2019
Nerve growth factor expression in mouse submandibular gland cells in vitro. Abstract and poster p... more Nerve growth factor expression in mouse submandibular gland cells in vitro. Abstract and poster presentation at The 4th Southern Ontario Neurosciences Association Meeting, London Ontario, CDA May 5, 199
Molecular and Cellular Biochemistry, Oct 1, 1987
Drug Development Research, Mar 18, 2021
Aberrant neural connectivity and intra‐cortical inhibitory dysfunction are key features of autism... more Aberrant neural connectivity and intra‐cortical inhibitory dysfunction are key features of autism. Non‐invasive brain stimulation (NIBS) protocols have been proposed that modulate this aberrant plasticity. However, additional investigations are needed to evaluate the impact of this intervention on biological biomarkers of the disease. We recently demonstrated alterations in serum insulin‐like growth factor‐1 (IGF‐1) and brain‐derived neurotrophic factor (BDNF) immunoreactivity in subjects with autism compared to controls. The aim of this pilot study was to explore the change in serum levels of the neurotrophic factors BDNF and IGF‐1 in patients undergoing NIBS therapy. Sixteen subjects with autism spectrum disorder (ASD) were tested 1 week before and 1 week after NIBS to determine the short‐term outcome on behavior using the total score on the autism behavior checklist, autism treatment evaluation checklist, clinical global impression severity and the autism diagnostic interview. ASD subjects younger than 11 years old (n = 11) were treated with transcranial direct current stimulation (tDCS), and those 11 years and older (n = 5) were treated with repetitive transcranial magnetic stimulation (rTMS). Serum levels of BDNF and IGF‐1 were evaluated by Enzyme‐Linked Immuno‐Sorbent Assay before and after the intervention with NIBS. A significant reduction in scores on the clinical behavioral scales was observed in patients treated with NIBS (ABC‐T p = .002, CGI‐S p = .008, ADI‐T and ATEC‐T p < .0001). There was a trend towards reduced serum BDNF levels after NIBS (p = .061), while there was no change in IGF‐1 levels. These data support further studies on the potential of BDNF as a biomarker to measure the effectiveness of NIBS in autism.
Neuroscience, Mar 1, 2021
Exercise is a promising, cost-effective intervention to augment successful aging and neurorehabil... more Exercise is a promising, cost-effective intervention to augment successful aging and neurorehabilitation. Decline of gray and white matter accompanies physiological aging and contributes to motor deficits in older adults. Exercise is believed to reduce atrophy within the motor system and induce neuroplasticity which in turn helps preserve motor function during aging and promote re-learning of motor skills, for example after stroke. To fully exploit the benefits of exercise, it is crucial to gain a greater understanding of the neurophysiological and molecular mechanisms underlying exercise-induced brain changes that prime neuroplasticity and thus contribute to postponing, slowing and ameliorating age- and disease-related impairments in motor function. This knowledge will allow us to develop more effective, personalized exercise protocols that meet individual needs, thereby increasing the utility of exercise strategies in clinical and non-clinical settings. Here, we review findings from studies that investigated neurophysiological and molecular changes associated with acute or long-term exercise in healthy, young adults and in healthy, postmenopausal women.
Learning & Memory, Nov 15, 2017
Physiological Reports, Jun 1, 2019
Neuroscience, Jun 1, 2020
Exercise induces neuroplasticity in descending motor pathways facilitating motor learning, and as... more Exercise induces neuroplasticity in descending motor pathways facilitating motor learning, and as such it could be utilized as an intervention in neurorehabilitation, for example when re-learning motor skills after stroke. To date, however, the neurophysiological and molecular mechanisms underlying exercise-induced neuroplasticity remain largely unknown impeding the potential utilization of exercise protocols as 'motor learning boosters' in clinical and non-clinical settings. Here, we assessed corticospinal excitability, intracortical facilitation (ICF) and short-interval intracortical inhibition (SICI) using transcranial magnetic stimulation (TMS) and serum biochemical markers including brain-derived neurotrophic factor (BDNF), total and precursor cathepsin B (tCTSB, proCTSB), uncarboxylated and carboxylated osteocalcin (unOCN, cOCN) and irisin using ELISA. Measurements were carried out in sedentary, healthy males before and after a single session of high-intensity interval exercise (HIIE) or in individuals who rested and did not perform exercise (No Exercise). We found that HIIE increased corticospinal excitability, BDNF and unOCN, and decreased cOCN. We also determined that greater increases in BDNF were associated with increases in unOCN and irisin and decreases in cOCN only in participants who underwent HIIE, suggesting that unOCN and irisin may contribute to exercise-induced BDNF increases. Conversely, no changes other than a decrease in serum unOCN/tOCN were found in No Exercise participants. The present findings show that a single session of HIIE is sufficient to modulate corticospinal excitability and to increase BDNF and unOCN in sedentary, healthy males.
Journal of Immunology, May 1, 2022
Sex-dependent discrepancies in disease prevalence and serum autoantibody levels are observed in p... more Sex-dependent discrepancies in disease prevalence and serum autoantibody levels are observed in patients and animal models of Alzheimer’s disease (AD). The present study examines whether gonadal hormones play a role in sex differences in serum autoantibody levels in the 3×Tg-AD mouse model of AD. 3×Tg-AD and wild-type (WT) mice were gonadectomised or sham-operated at 3 months of age. After behavioural phenotyping at 6 months of age, the animals were assessed for serum autoantibodies by indirect immunofluorescence for antinuclear antibodies (ANA) and by line-immunoblot assay for an additional 16 monospecific autoantibodies including anti-nucleosome antibodies. There were significant differences between the strains in ANA levels, with the major target antigens confirmed as nucleosomes. The results of ANA and anti-nucleosome assays were combined for further analysis. Further analysis revealed: 1) the level of serum autoantibodies in male 3×Tg-AD mice was higher than in female 3×Tg-AD animals, and this was not altered by orchiectomy. 2) sham-operated 3×Tg-AD female mice displayed a significantly lower level of serum autoantibodies than sham-operated WT females. 3) ovariectomy further reduced the level of serum autoantibodies in female 3×Tg-AD mice. The results suggest that dissimilar levels of serum autoantibodies in 3xTg-AD mice are a sex-dependent phenomenon and that female hormones play a role in regulation of their synthesis. Funded by grant #SVB-158618 from the Canadian Institutes of Health Research to MF.
Alzheimers & Dementia, Jul 1, 2017
Nucleic Acids Research, 1986
Journal of Bacteriology, Feb 1, 1979
International Journal of Molecular Sciences, Mar 9, 2017
Journal of comparative neurology, Jul 19, 2011
Journal of Neurosurgery, Nov 1, 2008
Progress in Neurobiology, May 1, 2004
Frontiers in Neuroscience, Feb 22, 2019
Neurobiology of Aging, Aug 1, 2015
Molecular Brain Research, Nov 1, 1996
Brain Research, Nov 1, 1993
Alzheimers & Dementia, Jul 1, 2019
Nerve growth factor expression in mouse submandibular gland cells in vitro. Abstract and poster p... more Nerve growth factor expression in mouse submandibular gland cells in vitro. Abstract and poster presentation at The 4th Southern Ontario Neurosciences Association Meeting, London Ontario, CDA May 5, 199
Molecular and Cellular Biochemistry, Oct 1, 1987
Drug Development Research, Mar 18, 2021
Aberrant neural connectivity and intra‐cortical inhibitory dysfunction are key features of autism... more Aberrant neural connectivity and intra‐cortical inhibitory dysfunction are key features of autism. Non‐invasive brain stimulation (NIBS) protocols have been proposed that modulate this aberrant plasticity. However, additional investigations are needed to evaluate the impact of this intervention on biological biomarkers of the disease. We recently demonstrated alterations in serum insulin‐like growth factor‐1 (IGF‐1) and brain‐derived neurotrophic factor (BDNF) immunoreactivity in subjects with autism compared to controls. The aim of this pilot study was to explore the change in serum levels of the neurotrophic factors BDNF and IGF‐1 in patients undergoing NIBS therapy. Sixteen subjects with autism spectrum disorder (ASD) were tested 1 week before and 1 week after NIBS to determine the short‐term outcome on behavior using the total score on the autism behavior checklist, autism treatment evaluation checklist, clinical global impression severity and the autism diagnostic interview. ASD subjects younger than 11 years old (n = 11) were treated with transcranial direct current stimulation (tDCS), and those 11 years and older (n = 5) were treated with repetitive transcranial magnetic stimulation (rTMS). Serum levels of BDNF and IGF‐1 were evaluated by Enzyme‐Linked Immuno‐Sorbent Assay before and after the intervention with NIBS. A significant reduction in scores on the clinical behavioral scales was observed in patients treated with NIBS (ABC‐T p = .002, CGI‐S p = .008, ADI‐T and ATEC‐T p < .0001). There was a trend towards reduced serum BDNF levels after NIBS (p = .061), while there was no change in IGF‐1 levels. These data support further studies on the potential of BDNF as a biomarker to measure the effectiveness of NIBS in autism.
Neuroscience, Mar 1, 2021
Exercise is a promising, cost-effective intervention to augment successful aging and neurorehabil... more Exercise is a promising, cost-effective intervention to augment successful aging and neurorehabilitation. Decline of gray and white matter accompanies physiological aging and contributes to motor deficits in older adults. Exercise is believed to reduce atrophy within the motor system and induce neuroplasticity which in turn helps preserve motor function during aging and promote re-learning of motor skills, for example after stroke. To fully exploit the benefits of exercise, it is crucial to gain a greater understanding of the neurophysiological and molecular mechanisms underlying exercise-induced brain changes that prime neuroplasticity and thus contribute to postponing, slowing and ameliorating age- and disease-related impairments in motor function. This knowledge will allow us to develop more effective, personalized exercise protocols that meet individual needs, thereby increasing the utility of exercise strategies in clinical and non-clinical settings. Here, we review findings from studies that investigated neurophysiological and molecular changes associated with acute or long-term exercise in healthy, young adults and in healthy, postmenopausal women.
Learning & Memory, Nov 15, 2017
Physiological Reports, Jun 1, 2019
Neuroscience, Jun 1, 2020
Exercise induces neuroplasticity in descending motor pathways facilitating motor learning, and as... more Exercise induces neuroplasticity in descending motor pathways facilitating motor learning, and as such it could be utilized as an intervention in neurorehabilitation, for example when re-learning motor skills after stroke. To date, however, the neurophysiological and molecular mechanisms underlying exercise-induced neuroplasticity remain largely unknown impeding the potential utilization of exercise protocols as 'motor learning boosters' in clinical and non-clinical settings. Here, we assessed corticospinal excitability, intracortical facilitation (ICF) and short-interval intracortical inhibition (SICI) using transcranial magnetic stimulation (TMS) and serum biochemical markers including brain-derived neurotrophic factor (BDNF), total and precursor cathepsin B (tCTSB, proCTSB), uncarboxylated and carboxylated osteocalcin (unOCN, cOCN) and irisin using ELISA. Measurements were carried out in sedentary, healthy males before and after a single session of high-intensity interval exercise (HIIE) or in individuals who rested and did not perform exercise (No Exercise). We found that HIIE increased corticospinal excitability, BDNF and unOCN, and decreased cOCN. We also determined that greater increases in BDNF were associated with increases in unOCN and irisin and decreases in cOCN only in participants who underwent HIIE, suggesting that unOCN and irisin may contribute to exercise-induced BDNF increases. Conversely, no changes other than a decrease in serum unOCN/tOCN were found in No Exercise participants. The present findings show that a single session of HIIE is sufficient to modulate corticospinal excitability and to increase BDNF and unOCN in sedentary, healthy males.
Journal of Immunology, May 1, 2022
Sex-dependent discrepancies in disease prevalence and serum autoantibody levels are observed in p... more Sex-dependent discrepancies in disease prevalence and serum autoantibody levels are observed in patients and animal models of Alzheimer’s disease (AD). The present study examines whether gonadal hormones play a role in sex differences in serum autoantibody levels in the 3×Tg-AD mouse model of AD. 3×Tg-AD and wild-type (WT) mice were gonadectomised or sham-operated at 3 months of age. After behavioural phenotyping at 6 months of age, the animals were assessed for serum autoantibodies by indirect immunofluorescence for antinuclear antibodies (ANA) and by line-immunoblot assay for an additional 16 monospecific autoantibodies including anti-nucleosome antibodies. There were significant differences between the strains in ANA levels, with the major target antigens confirmed as nucleosomes. The results of ANA and anti-nucleosome assays were combined for further analysis. Further analysis revealed: 1) the level of serum autoantibodies in male 3×Tg-AD mice was higher than in female 3×Tg-AD animals, and this was not altered by orchiectomy. 2) sham-operated 3×Tg-AD female mice displayed a significantly lower level of serum autoantibodies than sham-operated WT females. 3) ovariectomy further reduced the level of serum autoantibodies in female 3×Tg-AD mice. The results suggest that dissimilar levels of serum autoantibodies in 3xTg-AD mice are a sex-dependent phenomenon and that female hormones play a role in regulation of their synthesis. Funded by grant #SVB-158618 from the Canadian Institutes of Health Research to MF.
Alzheimers & Dementia, Jul 1, 2017
Nucleic Acids Research, 1986
Journal of Bacteriology, Feb 1, 1979