Hippocampal plasticity underpins long-term cognitive gains from resistance exercise in MCI
•Progressive resistance exercise leads to long-term cognitive benefits in MCI.•Resistance exercise slows post-training CA1, subiculum and dentate atrophy.•Within-training preservation of PCC predicts long-term hippocampal preservation.•Neuroprotection of AD-vulnerable hippocampal subfields mediate l...
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| Published in | NeuroImage clinical Vol. 25; p. 102182 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier Inc
01.01.2020
Elsevier |
| Subjects | |
| Online Access | Get full text |
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| Abstract | •Progressive resistance exercise leads to long-term cognitive benefits in MCI.•Resistance exercise slows post-training CA1, subiculum and dentate atrophy.•Within-training preservation of PCC predicts long-term hippocampal preservation.•Neuroprotection of AD-vulnerable hippocampal subfields mediate long-term cognition.•Long-term neuroprotection is not mediated by post-training fitness adaptations.
Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training.
One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures.
PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (p = 0.023, p = 0.020 and p = 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation.
Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia. |
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| AbstractList | •
Progressive resistance exercise leads to long-term cognitive benefits in MCI.
•
Resistance exercise slows post-training CA1, subiculum and dentate atrophy.
•
Within-training preservation of PCC predicts long-term hippocampal preservation.
•
Neuroprotection of AD-vulnerable hippocampal subfields mediate long-term cognition.
•
Long-term neuroprotection is not mediated by post-training fitness adaptations.
Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training.
One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures.
PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (
p
= 0.023,
p
= 0.020 and
p
= 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation.
Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia. Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training.One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures.PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (p = 0.023, p = 0.020 and p = 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation.Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia. Keywords: Resistance exercise, Mild cognitive impairment, Plasticity, Hippocampus, Subfields, Randomised controlled trial Highlights•Progressive resistance exercise leads to long-term cognitive benefits in MCI. •Resistance exercise slows post-training CA1, subiculum and dentate atrophy. •Within-training preservation of PCC predicts long-term hippocampal preservation. •Neuroprotection of AD-vulnerable hippocampal subfields mediate long-term cognition. •Long-term neuroprotection is not mediated by post-training fitness adaptations. •Progressive resistance exercise leads to long-term cognitive benefits in MCI.•Resistance exercise slows post-training CA1, subiculum and dentate atrophy.•Within-training preservation of PCC predicts long-term hippocampal preservation.•Neuroprotection of AD-vulnerable hippocampal subfields mediate long-term cognition.•Long-term neuroprotection is not mediated by post-training fitness adaptations. Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training. One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures. PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (p = 0.023, p = 0.020 and p = 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation. Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia. Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training. One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures. PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (p = 0.023, p = 0.020 and p = 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation. Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia.Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training. One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures. PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (p = 0.023, p = 0.020 and p = 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation. Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia. Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive impairment in older persons with lifestyle interventions continues to garner evidence but whether this can combat underlying neurodegeneration is unknown. The Study of Mental Activity and Resistance Training (SMART) trial has previously reported within-training findings; the aim of this study was to investigate the long-term neurostructural and cognitive impact of resistance exercise in Mild Cognitive Impairment (MCI). For the first time we show that hippocampal subareas particularly susceptible to volume loss in Alzheimer's disease (AD) are protected by resistance exercise for up to one year after training. One hundred MCI participants were randomised to one of four training groups: (1) Combined high intensity progressive resistance and computerised cognitive training (PRT+CCT), (2) PRT+Sham CCT, (3) CCT+Sham PRT, (4) Sham physical+sham cognitive training (SHAM+SHAM). Physical, neuropsychological and MRI assessments were carried out at baseline, 6 months (directly after training) and 18 months from baseline (12 months after intervention cessation). Here we report neuro-structural and functional changes over the 18-month trial period and the association with global cognitive and executive function measures. PRT but not CCT or PRT+CCT led to global long-term cognitive improvements above SHAM intervention at 18-month follow-up. Furthermore, hippocampal subfields susceptible to atrophy in AD were protected by PRT revealing an elimination of long-term atrophy in the left subiculum, and attenuation of atrophy in left CA1 and dentate gyrus when compared to SHAM+SHAM (p = 0.023, p = 0.020 and p = 0.027). These neuroprotective effects mediated a significant portion of long-term cognitive benefits. By contrast, within-training posterior cingulate plasticity decayed after training cessation and was unrelated to long term cognitive benefits. Neither general physical activity levels nor fitness change over the 18-month period mediated hippocampal trajectory, demonstrating that enduring hippocampal subfield plasticity is not a simple reflection of post-training changes in fitness or physical activity participation. Notably, resting-state fMRI analysis revealed that both the hippocampus and posterior cingulate participate in a functional network that continued to be upregulated following intervention cessation. Multiple structural mechanisms may contribute to the long-term global cognitive benefit of resistance exercise, developing along different time courses but functionally linked. For the first time we show that 6 months of high intensity resistance exercise is capable of not only promoting better cognition in those with MCI, but also protecting AD-vulnerable hippocampal subfields from degeneration for at least 12 months post-intervention. These findings emphasise the therapeutic potential of resistance exercise; however, future work will need to establish just how long-lived these outcomes are and whether they are sufficient to delay dementia. |
| ArticleNumber | 102182 |
| Author | Baker, Michael Li, Zhixiu Mavros, Yorgi Broadhouse, Kathryn M. Kochan, Nicole Valenzuela, Michael J. Singh, Maria Fiatarone Wen, Wei Singh, Nalin Wang, Yi Suo, Chao Gates, Nicola Brown, Matt Jain, Nidhi Sachdev, Perminder S. Brodaty, Henry Wilson, Guy C. Meiklejohn, Jacinda Baune, Bernhard T. Foroughi, Nasim Ashton, Kevin |
| AuthorAffiliation | e School of Psychological Sciences and Monash Biomedical Imaging, Monash University, Melbourne, VIC, Australia g Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, NSW, Australia h Neuropsychiatric Institute, Prince of Wales Hospital, Sydney, NSW, Australia p Institute of Health and Biomedical Innovation, Queensland University of Technology, QLD, Australia i Dementia Collaborative Research Centre, University of New South Wales, Sydney, NSW, Australia f School of Psychiatry, University of New South Wales, Sydney, NSW, Australia n Department of Medicine and the Diabetes Center, University of California, San Francisco, San Francisco, CA, USA q School of Medical Sciences, Sydney Medical School, University of Sydney, Sydney, NSW, Australia l School of Exercise Science, Australian Catholic University, Strathfield, NSW, Australia j Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences, The University of Sydney, |
| AuthorAffiliation_xml | – name: c Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences and Sydney Medical School, The University of Sydney, Lidcombe, NSW, Australia – name: h Neuropsychiatric Institute, Prince of Wales Hospital, Sydney, NSW, Australia – name: b Regenerative Neuroscience Group, Brain and Mind Centre and Sydney Medical School, The University of Sydney, Sydney, NSW, Australia – name: n Department of Medicine and the Diabetes Center, University of California, San Francisco, San Francisco, CA, USA – name: o Biomedical Sciences, Faculty of Health Sciences and Medicine, Bond University, QLD, Australia – name: p Institute of Health and Biomedical Innovation, Queensland University of Technology, QLD, Australia – name: d Hebrew SeniorLife and Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University, Boston, MA, USA – name: m Clinical and Rehabilitation Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – name: e School of Psychological Sciences and Monash Biomedical Imaging, Monash University, Melbourne, VIC, Australia – name: k Department of Psychiatry, School of Medicine, University of Adelaide, Adelaide, SA, Australia – name: a Nola Thompson Centre for Advanced Imaging, Sunshine Coast Mind and Neuroscience Thompson Institute, University of the Sunshine Coast, QLD, Australia – name: q School of Medical Sciences, Sydney Medical School, University of Sydney, Sydney, NSW, Australia – name: j Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – name: r King’s College London National Institutes of Health Biomedical Research Centre, UK – name: i Dementia Collaborative Research Centre, University of New South Wales, Sydney, NSW, Australia – name: l School of Exercise Science, Australian Catholic University, Strathfield, NSW, Australia – name: f School of Psychiatry, University of New South Wales, Sydney, NSW, Australia – name: g Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, NSW, Australia |
| Author_xml | – sequence: 1 givenname: Kathryn M. orcidid: 0000-0001-5168-9483 surname: Broadhouse fullname: Broadhouse, Kathryn M. email: kbroadhouse@usc.edu.au organization: Nola Thompson Centre for Advanced Imaging, Sunshine Coast Mind and Neuroscience Thompson Institute, University of the Sunshine Coast, QLD, Australia – sequence: 2 givenname: Maria Fiatarone surname: Singh fullname: Singh, Maria Fiatarone organization: Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences and Sydney Medical School, The University of Sydney, Lidcombe, NSW, Australia – sequence: 3 givenname: Chao surname: Suo fullname: Suo, Chao organization: Regenerative Neuroscience Group, Brain and Mind Centre and Sydney Medical School, The University of Sydney, Sydney, NSW, Australia – sequence: 4 givenname: Nicola surname: Gates fullname: Gates, Nicola organization: Regenerative Neuroscience Group, Brain and Mind Centre and Sydney Medical School, The University of Sydney, Sydney, NSW, Australia – sequence: 5 givenname: Wei surname: Wen fullname: Wen, Wei organization: School of Psychiatry, University of New South Wales, Sydney, NSW, Australia – sequence: 6 givenname: Henry surname: Brodaty fullname: Brodaty, Henry organization: Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, NSW, Australia – sequence: 7 givenname: Nidhi surname: Jain fullname: Jain, Nidhi organization: Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – sequence: 8 givenname: Guy C. surname: Wilson fullname: Wilson, Guy C. organization: Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – sequence: 9 givenname: Jacinda surname: Meiklejohn fullname: Meiklejohn, Jacinda organization: Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – sequence: 10 givenname: Nalin surname: Singh fullname: Singh, Nalin organization: Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – sequence: 11 givenname: Bernhard T. orcidid: 0000-0001-6548-426X surname: Baune fullname: Baune, Bernhard T. organization: Department of Psychiatry, School of Medicine, University of Adelaide, Adelaide, SA, Australia – sequence: 12 givenname: Michael surname: Baker fullname: Baker, Michael organization: Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences and Sydney Medical School, The University of Sydney, Lidcombe, NSW, Australia – sequence: 13 givenname: Nasim surname: Foroughi fullname: Foroughi, Nasim organization: Clinical and Rehabilitation Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – sequence: 14 givenname: Yi surname: Wang fullname: Wang, Yi organization: Clinical and Rehabilitation Research Group, Faculty of Health Sciences, The University of Sydney, Lidcombe, NSW, Australia – sequence: 15 givenname: Nicole surname: Kochan fullname: Kochan, Nicole organization: Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, NSW, Australia – sequence: 16 givenname: Kevin surname: Ashton fullname: Ashton, Kevin organization: Biomedical Sciences, Faculty of Health Sciences and Medicine, Bond University, QLD, Australia – sequence: 17 givenname: Matt surname: Brown fullname: Brown, Matt organization: Institute of Health and Biomedical Innovation, Queensland University of Technology, QLD, Australia – sequence: 18 givenname: Zhixiu surname: Li fullname: Li, Zhixiu organization: Institute of Health and Biomedical Innovation, Queensland University of Technology, QLD, Australia – sequence: 19 givenname: Yorgi orcidid: 0000-0002-2588-0425 surname: Mavros fullname: Mavros, Yorgi organization: Physical Activity, Lifestyle, Ageing and Wellbeing Faculty Research Group, Faculty of Health Sciences and Sydney Medical School, The University of Sydney, Lidcombe, NSW, Australia – sequence: 20 givenname: Perminder S. surname: Sachdev fullname: Sachdev, Perminder S. organization: Centre for Healthy Brain Ageing, School of Psychiatry, University of New South Wales, Sydney, NSW, Australia – sequence: 21 givenname: Michael J. surname: Valenzuela fullname: Valenzuela, Michael J. email: michael.valenzuela@sydney.edu.au organization: Regenerative Neuroscience Group, Brain and Mind Centre and Sydney Medical School, The University of Sydney, Sydney, NSW, Australia |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/31978826$$D View this record in MEDLINE/PubMed |
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| Snippet | •Progressive resistance exercise leads to long-term cognitive benefits in MCI.•Resistance exercise slows post-training CA1, subiculum and dentate... Highlights•Progressive resistance exercise leads to long-term cognitive benefits in MCI. •Resistance exercise slows post-training CA1, subiculum and dentate... Dementia affects 47 million individuals worldwide, and assuming the status quo is projected to rise to 150 million by 2050. Prevention of age-related cognitive... • Progressive resistance exercise leads to long-term cognitive benefits in MCI. • Resistance exercise slows post-training CA1, subiculum and dentate atrophy. •... |
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| SubjectTerms | Aged Cognitive Dysfunction - diagnostic imaging Cognitive Dysfunction - pathology Cognitive Dysfunction - physiopathology Cognitive Dysfunction - rehabilitation Cognitive Remediation Combined Modality Therapy Connectome Female Hippocampus Hippocampus - diagnostic imaging Hippocampus - pathology Hippocampus - physiopathology Humans Longitudinal Studies Male Middle Aged Mild cognitive impairment Nerve Net - diagnostic imaging Nerve Net - pathology Nerve Net - physiopathology Neuronal Plasticity - physiology Outcome Assessment, Health Care Placebos Plasticity Radiology Randomised controlled trial Regular Resistance exercise Resistance Training Subfields |
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| Title | Hippocampal plasticity underpins long-term cognitive gains from resistance exercise in MCI |
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