Journal ArticleDOI
BDNF-based synaptic repair as a disease-modifying strategy for neurodegenerative diseases
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TLDR
The key issues in translating BDNF biology into synaptic repair therapies are reviewed, which pave the way for a 'synaptic repair' therapy for neurodegenerative diseases that targets pathophysiology rather than pathogenesis.Abstract:
Synaptic dysfunction is a key pathophysiological hallmark in several neurodegenerative disorders. In this Review, Lu and colleagues consider a 'synaptic repair'-based therapy for neurodegenerative diseases that targets pathophysiology rather than pathogenesis and discuss BDNF as a potential synaptic repair molecule.read more
Citations
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Control of Brain Development, Function, and Behavior by the Microbiome
TL;DR: Emerging evidence that the microbiome extends its influence to the brain via various pathways connecting the gut to the central nervous system is highlighted.
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The Gut Microbiota and Alzheimer’s Disease
TL;DR: The purpose of this review is to summarize and discuss the current findings that may elucidate the role of the gut microbiota in the development of AD and to provide new insights into novel therapeutic strategies for AD.
Journal ArticleDOI
Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis
TL;DR: Research on the pathological mechanisms of neuroaxonal dysfunction and injury, such as altered ion channel activity, and the endogenous neuroprotective pathways that counteract oxidative stress and mitochondrial dysfunction are reviewed to identify potential novel therapeutic targets in MS.
Journal ArticleDOI
Microbiota-Brain-Gut Axis and Neurodegenerative Diseases
TL;DR: In theory, a role for the microbiota-gut-brain axis is highly plausible; clinical confirmation is awaited and a theoretical basis can be developed for the use of microbiota-directed therapies in neurodegenerative disorders.
Journal ArticleDOI
Exercise promotes the expression of brain derived neurotrophic factor (BDNF) through the action of the ketone body β-hydroxybutyrate
Sama F. Sleiman,Jeffrey Henry,Rami Al-Haddad,Lauretta El Hayek,Edwina Abou Haidar,Thomas Stringer,Devyani Ulja,Saravanan S. Karuppagounder,Edward B. Holson,Rajiv R. Ratan,Ipe Ninan,Moses V. Chao +11 more
TL;DR: An endogenous mechanism to explain how physical exercise leads to the induction of BDNF is revealed, and electrophysiological measurements indicate that β-hydroxybutyrate causes an increase in neurotransmitter release, which is dependent upon the TrkB receptor.
References
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Journal ArticleDOI
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Karen Hsiao,Paul F. Chapman,Steven P. Nilsen,Chris Eckman,Yasuo Harigaya,Steven G. Younkin,Fusheng Yang,Greg M. Cole +7 more
TL;DR: Transgenic mice overexpressing the 695-amino acid isoform of human Alzheimer β-amyloid (Aβ) precursor protein containing a Lys670 → Asn, Met671 → Leu mutation had normal learning and memory but showed impairment by 9 to 10 months of age.
Journal ArticleDOI
Physical basis of cognitive alterations in Alzheimer's disease: synapse loss is the major correlate of cognitive impairment.
Robert D. Terry,Eliezer Masliah,David P. Salmon,Nelson Butters,Richard DeTeresa,Robert Hill,Lawrence A. Hansen,Robert Katzman +7 more
TL;DR: Both linear regressions and multivariate analyses correlating three global neuropsychological tests with a number of structural and neurochemical measurements performed on a prospective series of patients with Alzheimer's disease and 9 neuropathologically normal subjects reveal very powerful correlations with all three psychological assays.
Journal ArticleDOI
Alzheimer's Disease Is a Synaptic Failure
TL;DR: Mounting evidence suggests that this syndrome begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, and that the synaptic dysfunction is caused by diffusible oligomeric assemblies of the amyloid β protein.
Journal ArticleDOI
Triple-Transgenic Model of Alzheimer's Disease with Plaques and Tangles: Intracellular Aβ and Synaptic Dysfunction
Salvatore Oddo,Antonella Caccamo,Jason D. Shepherd,M. Paul Murphy,Todd E. Golde,Rakez Kayed,Raju Metherate,Mark P. Mattson,Yama Akbari,Frank M. LaFerla +9 more
TL;DR: The recapitulation of salient features of AD in these mice clarifies the relationships between Abeta, synaptic dysfunction, and tangles and provides a valuable model for evaluating potential AD therapeutics as the impact on both lesions can be assessed.
Journal ArticleDOI
The BDNF val66met polymorphism affects activity-dependent secretion of BDNF and human memory and hippocampal function
Michael F. Egan,Masami Kojima,Masami Kojima,Joseph H. Callicott,Terry E. Goldberg,Bhaskar Kolachana,Alessandro Bertolino,Eugene Zaitsev,Bert Gold,David Goldman,Michael Dean,Bai Lu,Daniel R. Weinberger +12 more
TL;DR: A role is demonstrated for BDNF and its val/met polymorphism in human memory and hippocampal function and it is suggested val/ met exerts these effects by impacting intracellular trafficking and activity-dependent secretion of BDNF.