Age-related changes in nigrostriatal dopaminergic function are accentuated in +/− brain-derived neurotrophic factor mice

Neuroscience ◽  
2004 ◽  
Vol 128 (1) ◽  
pp. 201-208 ◽  
Author(s):  
D.E. Dluzen ◽  
J.L. McDermott ◽  
L.I. Anderson ◽  
J. Kucera ◽  
J.N. Joyce ◽  
...  
2006 ◽  
Vol 2 ◽  
pp. S103-S103
Author(s):  
Olaf Schulte-Herbrüggen ◽  
Uwe Deicke ◽  
Uwe Otten ◽  
Dorothee Abramowski ◽  
Matthias Staufenbiel ◽  
...  

2014 ◽  
Vol 15 (1) ◽  
pp. 38-44 ◽  
Author(s):  
Jagadeesh Rao ◽  
Joshua Chiappelli ◽  
Peter Kochunov ◽  
William T. Regenold ◽  
Stanley I. Rapoport ◽  
...  

2008 ◽  
Vol 12 (01) ◽  
pp. 137 ◽  
Author(s):  
Lakshmi N. Yatham ◽  
Flavio Kapczinski ◽  
Ana C. Andreazza ◽  
L. Trevor Young ◽  
Raymond W. Lam ◽  
...  

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Yoshito Mizoguchi ◽  
Hiroshi Yao ◽  
Yoshiomi Imamura ◽  
Manabu Hashimoto ◽  
Akira Monji

Abstract The beneficial effects of brain-derived neurotrophic factor (BDNF)—a member of the neurotrophin family—on cognitive function or dementia are well established in both rodents and human beings. In contrast, little is known about the association of proBDNF—a precursor protein with opposing neuronal effects of BDNF—with cognitive function in non-demented older adults. We analyzed brain magnetic resonance imaging findings of 256 community-dwelling older adults (mean age of 68.4 years). Serum BDNF and proBDNF levels were measured by quantitative enzyme-linked immunosorbent assay. Logistic regression analysis revealed that older age, less physical activity, hippocampal atrophy, and lower BDNF levels were independently associated with memory impairment determined by the Rivermead Behavioral Memory Test. Path analysis based on structural equation modeling indicated that age, sport activity, hippocampal atrophy and BDNF but not proBDNF were individually associated with Rivermead Behavioral Memory Test scores. These findings suggest that impaired BDNF function, in addition to physical inactivity and hippocampal atrophy, is associated with age-related memory impairment. Therefore, BDNF may be a potential target for dementia prevention.


2022 ◽  
Vol 0 (0) ◽  
Author(s):  
Shaun Cade ◽  
Xin-Fu Zhou ◽  
Larisa Bobrovskaya

Abstract Alzheimer’s disease is a neurodegenerative condition that is potentially mediated by synaptic dysfunction before the onset of cognitive impairments. The disease mostly affects elderly people and there is currently no therapeutic which halts its progression. One therapeutic strategy for Alzheimer’s disease is to regenerate lost synapses by targeting mechanisms involved in synaptic plasticity. This strategy has led to promising drug candidates in clinical trials, but further progress needs to be made. An unresolved problem of Alzheimer’s disease is to identify the molecular mechanisms that render the aged brain susceptible to synaptic dysfunction. Understanding this susceptibility may identify drug targets which could halt, or even reverse, the disease’s progression. Brain derived neurotrophic factor is a neurotrophin expressed in the brain previously implicated in Alzheimer’s disease due to its involvement in synaptic plasticity. Low levels of the protein increase susceptibility to the disease and post-mortem studies consistently show reductions in its expression. A desirable therapeutic approach for Alzheimer’s disease is to stimulate the expression of brain derived neurotrophic factor and potentially regenerate lost synapses. However, synthesis and secretion of the protein are regulated by complex activity-dependent mechanisms within neurons, which makes this approach challenging. Moreover, the protein is synthesised as a precursor which exerts the opposite effect of its mature form through the neurotrophin receptor p75NTR. This review will evaluate current evidence on how age-related alterations in the synthesis, processing and signalling of brain derived neurotrophic factor may increase the risk of Alzheimer’s disease.


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