Age-dependent effects of valproic acid in Alzheimer’s disease (AD) mice are associated with nerve growth factor (NGF) regulation

Noh, Hyun Ho; Seo, Hyemyung

doi:10.1016/j.neuroscience.2014.02.012

Cited by 34 publications

(19 citation statements)

References 55 publications

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“…Already it has been found that treatment with valproate (VPA) in animals with AD decreased the nuclear factor kappa B (NFкB) of IL-1β mRNA. VPA has also increased NGF levels in the hippocampus of animals that were 5 and 10 months of age [81]. Moreover, it is important emphasize that amyloid β blocks neuronal function via the inhibition of kinesin 5, consequently reducing the transport of cellsurface NGF/NTR(p75) in PC 12 cells [82].…”

Section: Ngf and Alzheimer's Diseasementioning

confidence: 99%

The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease

Budni¹,

Bellettini-Santos²,

Mina³

et al. 2015

Aging and disease

324

185

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Aging is a normal physiological process accompanied by cognitive decline. This aging process has been the primary risk factor for development of aging-related diseases such as Alzheimer's disease (AD). Cognitive deficit is related to alterations of neurotrophic factors level such as brain-derived neurotrophic factor (BDNF), nerve growth factor (NGF) and glial cellderived neurotrophic factor (GDNF). These strong relationship between aging and AD is important to investigate the time which they overlap, as well as, the pathophysiological mechanism in each event. Considering that aging and AD are related to cognitive impairment, here we discuss the involving these neurotrophic factors in the aging process and AD.

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Section: Ngf and Alzheimer's Diseasementioning

confidence: 99%

The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease

Budni¹,

Bellettini-Santos²,

Mina³

et al. 2015

Aging and disease

324

185

View full text Add to dashboard Cite

show abstract

“…The study by Noh H et al classified the pathogenic process into three different disease stages and sought therapeutic regimen from various angles in detail. They found administration of valproic acid (VPA) to inhibit HDAC reduced cytokine expression levels, raised sAPP and nerve growth factor (NGF) and finally enhanced cognitive function in Tg6799 AD mice [36]. AD in different progress stages may produce specific markers and stage-intervention targeted therapy would be a optimal choice.…”

Section: Strategies To Improve Drug Efficacymentioning

confidence: 99%

The development prospection of HDAC inhibitors as a potential therapeutic direction in Alzheimer’s disease

Yang

Zhang

Wang

et al. 2017

Transl Neurodegener

112

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Alzheimer’s disease (AD) is a chronic neurodegenerative disease, which is associated with learning and memory impairment in the elderly. Recent studies have found that treating AD in the way of chromatin remodeling via histone acetylation is a promising therapeutic regimen. In a number of recent studies, inhibitors of histone deacetylase (HDACs) have been found to be a novel promising therapeutic agents for neurological disorders, particularly for AD and other neurodegenerative diseases. Although HDAC inhibitors have the ability to ameliorate cognitive impairment, successful treatments in the classic AD animal model are rarely translated into clinical trials. As for the reduction of unwanted side effects, the development of HDAC inhibitors with increased isoform selectivity or seeking other directions is a key issue that needs to be addressed. The review focused on literatures on epigenetic mechanisms in recent years, especially on histone acetylation in terms of the enhancement of specificity, efficacy and avoiding side effects for treating AD.

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“…Moreover, HDAC inhibitors possess antidepressant properties in rodents as well as complementary procognitive actions also associated with neurodegenerative disease (Graff and Mansuy, 2008;Covington et al, 2009;Day and Sweatt, 2011;Lin et al, 2012;Yamawaki et al, 2012;Graff and Tsai, 2013;Noh and Seo, 2014). This is particularly important in depression, because cognitive dysfunctions have long been recognized as an intrinsic characteristic of major depressive disorder (Conradi et al, 2011;Millan et al, 2012) and represent the most common residual symptoms in partial responders (Gotlib and Joormann, 2010).…”

Section: Trd: Neurobiology and Identification Of Novel Targetsmentioning

confidence: 99%

International Union of Basic and Clinical Pharmacology CIV: The Neurobiology of Treatment-resistant Depression: From Antidepressant Classifications to Novel Pharmacological Targets

et al. 2018

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Major depressive disorder is one of the most prevalent and life-threatening forms of mental illnesses and a major cause of morbidity worldwide. Currently available antidepressants are effective for most patients, although around 30% are considered treatment resistant (TRD), a condition that is associated with a significant impairment of cognitive function and poor quality of life. In this respect, the identification of the molecular mechanisms contributing to TRD represents an essential step for the design of novel and more efficacious drugs able to modify the clinical course of this disorder and increase remission rates in clinical practice. New insights into the neurobiology of TRD have shed light on the role of a number of different mechanisms, including the glutamatergic system, immune/inflammatory systems, neurotrophin function, and epigenetics. Advances in drug discovery processes in TRD have also influenced the classification of antidepressant drugs and novel classifications are available, such as the neuroscience-based nomenclature that can incorporate such advances in drug development for TRD. This review aims to provide an up-to-date description of key mechanisms in TRD and describe current therapeutic strategies for TRD before examining novel approaches that may ultimately address important neurobiological mechanisms not targeted by currently available antidepressants. All in all, we suggest that drug targeting different neurobiological systems should be able to restore normal function but must also promote resilience to reduce the long-term vulnerability to recurrent depressive episodes.

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Age-dependent effects of valproic acid in Alzheimer’s disease (AD) mice are associated with nerve growth factor (NGF) regulation

Cited by 34 publications

References 55 publications

The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease

The involvement of BDNF, NGF and GDNF in aging and Alzheimer's disease

The development prospection of HDAC inhibitors as a potential therapeutic direction in Alzheimer’s disease

International Union of Basic and Clinical Pharmacology CIV: The Neurobiology of Treatment-resistant Depression: From Antidepressant Classifications to Novel Pharmacological Targets

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