TY  - JOUR
A1  - Maass, Anne
A1  - Düzel, Sandra
A1  - Brigadski, Tanja
A1  - Goerke, Monique
A1  - Becke, Andreas
A1  - Sobieray, Uwe
A1  - Neumann, Katja
A1  - Lövdén, Martin
A1  - Lindenberger, Ulman
A1  - Bäckman, Lars
A1  - Braun-Dullaeus, Rüdiger
A1  - Ahrens, Dörte
A1  - Heinze, Hans-Jochen
A1  - Müller, Notger G.
A1  - Lessmann, Volkmar
A1  - Sendtner, Michael
A1  - Düzel, Emrah
T1  - Relationships of peripheral IGF-1, VEGF and BDNF levels to exercise-related changes in memory, hippocampal perfusion and volumes in older adults
JF  - NeuroImage
N2  - Animal models point towards a key role of brain-derived neurotrophic factor (BDNF), insulin-like growth factor-I (IGF-I) and vascular endothelial growth factor (VEGF) in mediating exercise-induced structural and functional changes in the hippocampus. Recently, also platelet derived growth factor-C (PDGF-C) has been shown to promote blood vessel growth and neuronal survival. Moreover, reductions of these neurotrophic and angiogenic factors in old age have been related to hippocampal atrophy, decreased vascularization and cognitive decline. In a 3-month aerobic exercise study, forty healthy older humans (60 to 77 years) were pseudo-randomly assigned to either an aerobic exercise group (indoor treadmill, n = 21) or to a control group (indoor progressive-muscle relaxation/stretching, n = 19). As reported recently, we found evidence for fitness-related perfusion changes of the aged human hippocampus that were closely linked to changes in episodic memory function. Here, we test whether peripheral levels of BDNF, IGF-I, VEGF or PDGF-C are related to changes in hippocampal blood flow, volume and memory performance. Growth factor levels were not significantly affected by exercise, and their changes were not related to changes in fitness or perfusion. However, changes in IGF-I levels were positively correlated with hippocampal volume changes (derived by manual volumetry and voxel-based morphometry) and late verbal recall performance, a relationship that seemed to be independent of fitness, perfusion or their changes over time. These preliminary findings link IGF-I levels to hippocampal volume changes and putatively hippocampus-dependent memory changes that seem to occur over time independently of exercise. We discuss methodological shortcomings of our study and potential differences in the temporal dynamics of how IGF-1, VEGF and BDNF may be affected by exercise and to what extent these differences may have led to the negative findings reported here.
KW  - Exercise
KW  - Neurotrophic factors
KW  - Hippocampus
KW  - Vascular plasticity
KW  - Aging
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-189219
VL  - 131
ER  - 
TY  - JOUR
A1  - Düzel, Emrah
A1  - van Praag, Henriette
A1  - Sendtner, Michael
T1  - Can physical exercise in old age improve memory and hippocampal function?
JF  - Brain
N2  - Physical exercise can convey a protective effect against cognitive decline in ageing and Alzheimer’s disease. While the long-term health-promoting and protective effects of exercise are encouraging, it’s potential to induce neuronal and vascular plasticity in the ageing brain is still poorly understood. It remains unclear whether exercise slows the trajectory of normal ageing by modifying vascular and metabolic risk factors and/or consistently boosts brain function by inducing structural and neurochemical changes in the hippocampus and related medial temporal lobe circuitry—brain areas that are important for learning and memory. Hence, it remains to be established to what extent exercise interventions in old age can improve brain plasticity above and beyond preservation of function. Existing data suggest that exercise trials aiming for improvement and preservation may require different outcome measures and that the balance between the two may depend on exercise intensity and duration, the presence of preclinical Alzheimer’s disease pathology, vascular and metabolic risk factors and genetic variability.
KW  - hippocampus
KW  - exercise
KW  - cerebral blood flow
KW  - Alzheimer's disease
KW  - memory
Y1  - 2016
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-190721
VL  - 139
IS  - 3
ER  -