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Potential therapeutic roles of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease

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Neural Regeneration Research 2019年第11期14卷 1880-1892页

作者： Bhaskar C. Das Somsankar Dasgupta Swapan K. Ray Department of Medicine Icahn School of Medicine at Mount SinaiNew YorkNYUSA Department of Neuroscience and Regenerative Medicine Institute of Molecular Medicine and GeneticsAugusta UniversityAugustaGAUSA Department of Pathology Microbiologyand ImmunologyUniversity of South Carolina School of MedicineColumbiaSCUSA

All retinoids, which can be natural and synthetic, are chemically related to vitamin A. Both natural and synthetic retinoids use specific nuclear receptors such as retinoic acid receptors and retinoid X receptors to activate specific signaling pathways in the cells. Retinoic acid signaling is extremely important in the central nervous system. Impairment of retinoic acid signaling pathways causes severe pathological processes in the central nervous system, especially in the adult brain. Retinoids have major roles in neural patterning, differentiation, axon outgrowth in normal development, and function of the brain. Impaired retinoic acid signaling results in neuroinflammation, oxidative stress, mitochondrial malfunction, and neurodegeneration leading to progressive Alzheimer’s disease, which is pathologically characterized by extra-neuronal accumulation of amyloid plaques(aggregated amyloid-beta) and intra-neurofibrillary tangles(hyperphosphorylated tau protein) in the temporal lobe of the brain. Alzheimer’s disease is the most common cause of dementia and loss of memory in old adults. Inactive cholinergic neurotransmission is responsible for cognitive deficits in Alzheimer’s disease patients. Deficiency or deprivation of retinoic acid in mice is associated with loss of spatial learning and memory. Retinoids inhibit expression of chemokines and neuroinflammatory cytokines in microglia and astrocytes, which are activated in Alzheimer’s disease. Stimulation of retinoic acid receptors and retinoid X receptors slows down accumulation of amyloids, reduces neurodegeneration, and thereby prevents pathogenesis of Alzheimer’s disease in mice. In this review, we described chemistry and biochemistry of some natural and synthetic retinoids and potentials of retinoids for prevention of neuroinflammation and neurodegeneration in Alzheimer’s disease.

关键词： Alzheimer's disease amyloid plaques neurofibrillary tangles neuroinflammation neurodegeneration retinoids

Development in the research of molecular mechanism of Alzheimer's disease

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Chinese Science Bulletin 1999年第14期44卷 1257-1264页

作者： Ming Gu Xiaomin Wang Yuanyue Mu Ming Fan Neuroscience Research Institute of Beijing Medical University Beijing China Basal Medicine Institute of Military Medical Academy Beijing China

Alzheimer’s disease (AD) is a kind of central nervous system disease. The cause of AD is unclear. It is found that the remarkable histopathological characters of AD are senile plaques and neurofibrillary tangles.β-amyloid plays an important role in the formation of senile plaques and the abnormal phosphorylation of Tau protein is the main reason of neurofibrillary tangles. Apolipoprotein E is correlated to AD’s access, and the third pathological characterAMY plaque perhaps represents a new cause of AD. Presenlin and proteinaceous infectious particles are also related with AD. A summary of molecular mechanism for AD and the development of research is presented.

关键词： Alzheimer’s disease senile plaque neurofibrillary tangles β-amyloid Tau protein apoliporprotein E presenlin proteinaceous infectious particles.

Longitudinal observation of ten family members with idiopathic basal ganglia calcification: A case report

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World Journal of Clinical Cases 2019年第12期7卷 1483-1491页

作者： Seiju Kobayashi Kumiko Utsumi Masaru Tateno Tomo Iwamoto Tomonori Murayama Hitoshi Sohma Wataru Ukai Eri Hashimoto Chiaki Kawanishi Shinyukai Nakae Hospital Sapporo 0010022 Japan Department of Neuropsychiatry Sapporo Medical University Graduate School of Medicine Sapporo 0608543 Japan Department of Psychiatry Sunagawa City Medical Center Sunagawa 0730196 Japan Tokiwa Child Development Center Tokiwa Hospital Sapporo Japan Department of Neuropsychiatry Sapporo Medical University Graduate School of Medicine Sapporo 0050853 Japan Department of Educational Development Sapporo Medical University Center for Medical Education Sapporo 0608543 Japan Department of Biomedical Engineering Sapporo Medical University School of Medicine Sapporo 0608543 Japan

BACKGROUND Familial idiopathic basal ganglia calcification (FIBGC) is a rare autosomal dominant disorder that causes bilateral calcification of the basal ganglia and/or cerebellar dentate nucleus, among other locations. CASE SUMMARY The aim of this study is to report 10 cases of FIBGC observed in a single family. Seven patients showed calcification on their computed tomography scan, and all of these patients carried the SLC20A2 mutation. However, individuals without the mutation did not show calcification. Three patients among the 7 with calcification were symptomatic, while the remaining 4 patients were asymptomatic. Additionally, we longitudinally observed 10 subjects for ten years. In this paper, we mainly focus on the clinical course and neuroradiological findings in the proband and her *** The accumulation of more case reports and further studies related to the manifestation of FIBGC are needed.

关键词： Idiopathic basal ganglia calcification Fahr’s disease SLC20A2 Diffuse neurofibrillary tangles with calcification Single-photon emission computed tomography Case report

Effects of 17-allylamino-17-demethoxygeldanamycin (17-AAG) in transgenic mouse models of frontotemporal lobar degeneration and Alzheimer’s disease

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Translational Neurodegeneration 2013年第1期2卷 174-182页

作者： Shuk Wai Ho Yuk Tung Chanel Tsui Ting Ting Wong Stanley Kwok-Kuen Cheung William B Goggins Lau Ming Yi Kwok Kin Cheng Larry Baum Department of Surgery The University of Hong KongPokfulamHong KongChina School of Biomedical Sciences(Pharmacology) The University of NottinghamNottinghamUK Department of Microbiology The University of Hong KongPokfulamHong KongChina School of Public Health and Primary Care The Chinese University of Hong KongShatinHong KongChina School of Pharmacy The Chinese University of Hong KongShatinHong KongChina

Alzheimer’s disease(AD),the most common dementia,is characterized by potentially neurotoxic aggregation of Aβ peptide and tau protein,and their deposition as amyloid plaques and neurofibrillary tangles(NFTs).Tau aggregation also occurs in other common neurodegenerative *** dementia(FTD)can be caused by tau mutations that increase the susceptibility of tau to hyperphosphorylation and aggregation,which may cause neuronal dysfunction and deposition of NFTs.17-allylamino-17-demethoxygeldanamycin(17-AAG)is a potent inhibitor of heat shock protein 90(Hsp90),a cytosolic chaperone implicated in the proper folding and functions of a repertoire of client proteins.17-AAG binds to Hsp90 and enhances degradation of Hsp90 client *** sought to determine whether 17-AAG can reduce Aβ and tau pathology in the brains of AD and FTD model mice expressing Aβ or P301L mutant tau,*** were randomized to receive 25,5,or 0 mg/kg 17-AAG thrice weekly from age eight to 11 *** was performed by rotarod test on motor function,on the area occupied by plaques in hippocampus or NFTs in medulla tissue sections,and on mortality.A high dose of 17-AAG tended to decrease NFTs in male mice(p=0.08).Further studies are required to confirm the effect of 17-AAG in diseases of tau aggregation.

关键词： Dementia Mouse tangles Plaques

Recent Advances in the Quest for Treatment and Management of Alzheimer and Other Dementia

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Open Journal of Medicinal Chemistry 2019年第1期9卷 1-35页

作者： Sameena E. Tanwir Ajay Kumar School of Science Technology and Environment Universidad Ana G. Mendez San Juan PR USA

Alzheimer’s disease (AD) is a neurodegenerative disease distinguished by progressive cognitive deterioration along with declining activities of daily living and behavioral changes. It is the commonest type of pre-senile and senile dementia. Many new therapeutic strategies have been developed in the last few years. We aimed at reviewing the evidence supporting these new therapeutic targets, including anti-amyloid and anti-Tau strategies. This review is focused on important future direction in investigation of potential therapeutic targets for AD drug discovery. Medical advances have improved treatment of many diseases but still there is a need to establish new tools for early diagnosis of AD. A thorough comprehensive understanding of the unexplored mechanism can ameliorate the diagnostic and therapeutic management of AD. There have been several disease-modifying therapeutic strategies for AD in the last few years and are presently at various phases of investigation. Few of them have shown promising results, but their safety and efficacy need to be further explored.

关键词： Alzheimer β Amyloid Tau Acetylcholinesterase Amyloid Precursor Protein Plaques tangles Neurodegeneration

The Growing Evidence for Photobiomodulation as a Promising Treatment for Alzheimer’s Disease

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Journal of Biosciences and Medicines 2018年第12期6卷 100-110页

作者： Lew Lim Vielight Inc. Toronto Canada

Despite the current belief that there is no effective treatment for Alzheimer’s Disease (AD), one emerging modality may change this belief: Photobiomodulation (PBM). It has credible mechanisms and growing evidence to support its case. Transcranial PBM for AD is a single intervention with multiple pathway mechanisms stemming from delivering low energy near infrared (NIR) light to the mitochondria in brain cells. The mechanisms involve the activation of gene transcription that lead to neuronal recovery, removal of toxic plaques, normalizing network oscillations that can lead to improved cognition and functionality. When PBM is delivered at 810 nm wavelength and pulsed at 40 Hz, early evidence suggests that very significant outcomes are possible. Literature related to PBM and AD has covered in vitro cellular, animal and human case reports, with promising results. They warrant robust randomized trials which are either ongoing or ready to start. The evidence in human studies is manifested in assessment scales such ADAS-cog, MMSE, and ADAS-ADL, and are supported by fMRI imaging and EEG.

关键词： Photobiomodulation Alzheimer’s Disease Near Infrared Light Default Mode Network Clinical Trials Aβ Neurofibrillary tangles Tau Neuro Gamma