Neuronal histamine and cognitive symptoms in Alzheimer's disease

Zlomuzica, Armin; Dere, Dorothea; Binder, Sonja; Silva, Maria Angélica de Souza; Huston, Joseph P.; Dere, Ekrem

doi:10.1016/j.neuropharm.2015.05.007

Cited by 79 publications

(55 citation statements)

References 152 publications

(178 reference statements)

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“…In a recent study, cognitive deficits were demonstrated along with changes in histaminergic neurotransmission [176, 177]. Higuchi et al also reported the correlation between H1R binding action and memory loss in AD patients of frontal and temporal regions, where they found decreased expression of H1 receptors [178].…”

Section: Neurotransmitter-based Therapeutics In Admentioning

confidence: 99%

“…Higuchi et al also reported the correlation between H1R binding action and memory loss in AD patients of frontal and temporal regions, where they found decreased expression of H1 receptors [178]. Interestingly, HDC and H1R knockout mice have also shown behavioral and neurochemical alterations [177, 179, 180]. Adult H1R deficient mice also exhibit the severe impairment in learning and memory, thus affecting both spatial and working memory [181, 182], novel objects [183], temporal order memory [184], and the retrieval of formed episodic memories [185].…”

Section: Neurotransmitter-based Therapeutics In Admentioning

confidence: 99%

“…H3R antagonists/inverse agonist molecules such as JNJ-10181457, Thioperamide, Clobenpropit, JNJ-5207852, Pitolisant, Spiro fused piperazine amides, ABT-288, GSK189254, SAR110894, and CEP-26401 are able to reverse partial lost cognitive functions in amnesia models of C57BL/6J mice, Wistar rats, Long-Evans rats, CD1/ICR mice, Sprague Dawley rats, CD-1 mice, and lister hooded rats [177]. The first H3R antagonist, i.e., pitolisant, was evaluated in human trials for treating narcolepsy patients [177, 190] and facilitates the consolidation of memory in mice [191, 192].…”

Section: Neurotransmitter-based Therapeutics In Admentioning

confidence: 99%

See 2 more Smart Citations

Therapeutics of Neurotransmitters in Alzheimer’s Disease

Kandimalla

Reddy

2017

JAD

187

143

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Alzheimer’s disease (AD) is a progressive neurodegenerative disease, characterized by the loss of memory, multiple cognitive impairments and changes in the personality and behavior. Several decades of intense research have revealed that multiple cellular changes are involved in disease process, including synaptic damage, mitochondrial abnormalities and inflammatory responses, in addition to formation and accumulation of amyloid-β (Aβ) and phosphorylated tau. Although tremendous progress has been made in understanding the impact of neurotransmitters in the progression and pathogenesis of AD, we still do not have a drug molecule associated with neurotransmitter(s) that can delay disease process in elderly individuals and/or restore cognitive functions in AD patients. The purpose of our article is to assess the latest developments in neurotransmitters research using cell and mouse models of AD. We also updated the current status of clinical trials using neurotransmitters’ agonists/antagonists in AD.

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Section: Neurotransmitter-based Therapeutics In Admentioning

confidence: 99%

Section: Neurotransmitter-based Therapeutics In Admentioning

confidence: 99%

Section: Neurotransmitter-based Therapeutics In Admentioning

confidence: 99%

See 1 more Smart Citation

Therapeutics of Neurotransmitters in Alzheimer’s Disease

Kandimalla

Reddy

2017

JAD

187

143

View full text Add to dashboard Cite

show abstract

“…While much of the research focuses on the cholinergic and glutamatergic pathways, recently scientists have proposed changes in a host of other neurotransmitters (174,175).…”

Section: Relevance To Alzheimer's Diseasementioning

confidence: 99%

Astrocytic transporters in Alzheimer's disease

Ugbode

Whalley

et al. 2017

Biochemical Journal

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Astrocytes play a fundamental role in maintaining the health and function of the central nervous system. Increasing evidence indicates that astrocytes undergo both cellular and molecular changes at an early stage in neurological diseases, including Alzheimer's disease (AD). These changes may reflect a change from a neuroprotective to a neurotoxic phenotype. Given the lack of current disease-modifying therapies for AD, astrocytes have become an interesting and viable target for therapeutic intervention. The astrocyte transport system covers a diverse array of proteins involved in metabolic support, neurotransmission and synaptic architecture. Therefore, specific targeting of individual transporter families has the potential to suppress neurodegeneration, a characteristic hallmark of AD. A small number of the 400 transporter superfamilies are expressed in astrocytes, with evidence highlighting a fraction of these are implicated in AD. Here, we review the current evidence for six astrocytic transporter subfamilies involved in AD, as reported in both animal and human studies. This review confirms that astrocytes are indeed a viable target, highlights the complexities of studying astrocytes and provides future directives to exploit the potential of astrocytes in tackling AD.

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“…Alzheimer's disease (AD), a severe age-related neurodegenerative disorder, is characterized by the accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles, synaptic and neuronal loss, and cognitive decline (1,2). An estimated 5.3 million Americans have AD; 5.1 million of these are aged 65 and over, and approximately 200,000 are <65 years-of-age and have younger onset AD (3).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

Zhang

Xing

Guo

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) are a class of endogenous small non-coding RNAs that have been revealed to negatively mediate the expression of their target genes at the post-transcriptional level. Recently, particular miRs have demonstrated an involvement in the pathogenesis of Alzheimer's disease (AD). However, the specific role of miR-135b in AD has yet to be elucidated. The present study aimed to investigate the neuroprotective role of miR-135b, in addition to its underlying mechanism. Herein, reverse transcription-quantitative polymerase chain reaction was conducted to determine miR-135b expression levels in the peripheral blood samples of patients with AD and age-matched normal controls. The data of the present study revealed that the expression levels of miR-135b were significantly reduced in the peripheral blood of AD patients compared with normal controls (P<0.01). In vitro MTT analyses identified that the overexpression of miR-135b significantly enhanced the proliferation of hippocampal cells (P<0.01). Furthermore, in vivo analysis using a Y-maze test indicated that injection with miR-135b mimics into the third ventricle of anesthetized SAMP8 mice significantly enhanced their learning and memory capacities (P<0.01). Molecular mechanism investigations identified β-site APP-cleaving enzyme 1 (BACE1) as a direct target gene of miR-135b, and the latter was identified to negatively mediate the protein expression levels of BACE1 in hippocampal cells, in addition to hippocampal tissues, of SAMP8 mice. Based on the aforementioned findings, we propose that miR-135b has a neuroprotective role via direct targeting of BACE1 and, thus, may be used for the treatment of AD.

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Neuronal histamine and cognitive symptoms in Alzheimer's disease

Cited by 79 publications

References 152 publications

Therapeutics of Neurotransmitters in Alzheimer’s Disease

Therapeutics of Neurotransmitters in Alzheimer’s Disease

Astrocytic transporters in Alzheimer's disease

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

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