Generic placeholder image

Current Pharmaceutical Design

Editor-in-Chief

ISSN (Print): 1381-6128
ISSN (Online): 1873-4286

Review Article

Exploring Potential of Alkaloidal Phytochemicals Targeting Neuroinflammatory Signaling of Alzheimer's Disease

Author(s): Md. Sahab Uddin*, Md. Tanvir Kabir, Abdullah Al Mamun, Tapan Behl, Rasha A. Mansouri, Akram Ahmed Aloqbi, Asma Perveen, Abdul Hafeez and Ghulam Md Ashraf*

Volume 27, Issue 3, 2021

Published on: 31 May, 2020

Page: [357 - 366] Pages: 10

DOI: 10.2174/1381612826666200531151004

Price: $65

Abstract

Alzheimer's disease (AD) is a chronic neurodegenerative disorder that is marked by cognitive dysfunctions and the existence of neuropathological hallmarks such as amyloid plaques, and neurofibrillary tangles. It has been observed that a persistent immune response in the brain has appeared as another neuropathological hallmark in AD. The sustained activation of the microglia, the brain’s resident macrophages, and other immune cells has been shown to aggravate both tau and amyloid pathology and may consider as a connection in the AD pathogenesis. However, the basic mechanisms that link immune responses in the pathogenesis of AD are unclear until now since the process of neuroinflammation can have either a harmful or favorable effect on AD, according to the phase of the disease. Numerous researches recommend that nutritional fruits, as well as vegetables, possess neurodefensive properties against the detrimental effects of neuroinflammation and aging. Moreover, these effects are controlled by diverse phytochemical compounds that are found in plants and demonstrate anti-inflammatory, neuroprotective, as well as other beneficial actions. In this review, we focus on the link of neuroinflammation in AD as well as highlight the probable mechanisms of alkaloidal phytochemicals to combat the neuroinflammatory aspect of AD.

Keywords: Alzheimer's disease, amyloid plaques, neurofibrillary tangles, alkaloidal phytochemicals, neuroinflammation, immune responses.

[1]
Uddin MS, Al Mamun A, Asaduzzaman M, et al. Spectrum of disease and prescription pattern for outpatients with neurological disorders: An empirical pilot study in Bangladesh. Ann Neurosci 2018; 25(1): 25-37.
[http://dx.doi.org/10.1159/000481812] [PMID: 29887680]
[2]
Al Mamun A, Uddin MS. KDS2010: A potent highly selective and reversible MAO-B inhibitor to abate Alzheimer’s disease. Comb Chem High Throughput Screen 2020; 23.
[http://dx.doi.org/10.2174/1386207323666200117103144] [PMID: 31957612]
[3]
Kabir MT, Uddin MS, Begum MM, et al. Cholinesterase inhibitors for Alzheimer’s disease: multitargeting strategy based on anti-alzheimer’s drugs repositioning. Curr Pharm Des 2019; 25(33): 3519-35.
[http://dx.doi.org/10.2174/1381612825666191008103141] [PMID: 31593530]
[4]
Caselli RJ, Beach TG, Yaari R, Reiman EM. Alzheimer’s disease a century later. J Clin Psychiatry 2006; 67(11): 1784-800.
[http://dx.doi.org/10.4088/JCP.v67n1118] [PMID: 17196061]
[5]
Hossain MF, Uddin MS, Uddin GMS, et al. Melatonin in Alzheimer’s disease: A latent endogenous regulator of neurogenesis to mitigate alzheimer’s neuropathology. Mol Neurobiol 2019; 56(12): 8255-76.
[http://dx.doi.org/10.1007/s12035-019-01660-3] [PMID: 31209782]
[6]
Zaplatic E, Bule M, Shah SZA, Uddin MS, Niaz K. Molecular mechanisms underlying protective role of quercetin in attenuating Alzheimer’s disease. Life Sci 2019; 224: 109-19.
[http://dx.doi.org/10.1016/j.lfs.2019.03.055] [PMID: 30914316]
[7]
Uddin MS, Rahman MM, Jakaria M, et al. Estrogen signaling in Alzheimer’s disease: molecular insights and therapeutic targets for alzheimer’s dementia. Mol Neurobiol 2020; 1-17.
[PMID: 32297302]
[8]
Kabir MT, Uddin MS, Mathew B, Das PK, Ashraf GM. Emerging promise of immunotherapy for Alzheimer’s disease: A new hope for the development of Alzheimer’s vaccine. Curr Top Med Chem 2020.
[http://dx.doi.org/10.2174/1568026620666200422105156] [PMID: 32321405]
[9]
Al Mamun A, Uddin MS, Kabir MT, et al. Exploring the promise of targeting ubiquitin-proteasome system to combat Alzheimer’s disease. Neurotox Res 2020; 1-10.
[http://dx.doi.org/10.1007/s12640-020-00185-1] [PMID: 32157628]
[10]
Uddin MS, Kabir MT, Rahman MH, et al. Exploring the multifunctional neuroprotective promise of rasagiline derivatives for multi-dysfunctional Alzheimer’s disease. Curr Pharm Des 2020; 26.
[http://dx.doi.org/10.2174/1381612826666200406075044] [PMID: 32250219]
[11]
Goedert M. Tau protein and the neurofibrillary pathology of Alzheimer’s disease. Trends Neurosci 1993; 16(11): 460-5.
[http://dx.doi.org/10.1016/0166-2236(93)90078-Z] [PMID: 7507619]
[12]
Uddin MS, Mamun AA, Jakaria M, et al. Emerging promise of sulforaphane-mediated Nrf2 signaling cascade against neurological disorders. Sci Total Environ 2020; 707135624
[http://dx.doi.org/10.1016/j.scitotenv.2019.135624] [PMID: 31784171]
[13]
Rahman MA, Rahman MR, Zaman T, et al. Emerging potential of naturally occurring autophagy modulators against neurodegeneration. Curr Pharm Des 2020; 26(7): 772-9.
[http://dx.doi.org/10.2174/1381612826666200107142541] [PMID: 31914904]
[14]
Serrano-Pozo A, Mielke ML, Gómez-Isla T, et al. Reactive glia not only associates with plaques but also parallels tangles in Alzheimer’s disease. Am J Pathol 2011; 179(3): 1373-84.
[http://dx.doi.org/10.1016/j.ajpath.2011.05.047] [PMID: 21777559]
[15]
Lambert J-C, Ibrahim-Verbaas CA, Harold D, et al. European Alzheimer’s Disease Initiative (EADI); genetic and environmental risk in alzheimer’s disease; alzheimer’s disease genetic consortium; cohorts for heart and aging research in genomic epidemiology. Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer’s disease. Nat Genet 2013; 45(12): 1452-8.
[http://dx.doi.org/10.1038/ng.2802] [PMID: 24162737]
[16]
Bu XL, Yao XQ, Jiao SS, et al. A study on the association between infectious burden and Alzheimer’s disease. Eur J Neurol 2015; 22(12): 1519-25.
[http://dx.doi.org/10.1111/ene.12477] [PMID: 24910016]
[17]
Budni J, Garcez ML, de Medeiros J, et al. The anti-inflammatory role of minocycline in Alzheimer’s disease. Curr Alzheimer Res 2016; 13(12): 1319-29.
[http://dx.doi.org/10.2174/1567205013666160819124206] [PMID: 27539598]
[18]
Zilka N, Kazmerova Z, Jadhav S, et al. Who fans the flames of Alzheimer’s disease brains? Misfolded tau on the crossroad of neurodegenerative and inflammatory pathways. J Neuroinflammation 2012; 9: 47.
[http://dx.doi.org/10.1186/1742-2094-9-47] [PMID: 22397366]
[19]
Tejera D, Heneka MT, Microglia M. Microglia in Alzheimer’s disease: the good, the bad and the ugly. Curr Alzheimer Res 2016; 13(4): 370-80.
[http://dx.doi.org/10.2174/1567205013666151116125012] [PMID: 26567746]
[20]
Jaturapatporn D, Isaac MGEKN, McCleery J, Tabet N. Aspirin, steroidal and non-steroidal anti-inflammatory drugs for the treatment of Alzheimer’s disease. Cochrane Database Syst Rev 2012; (2): CD006378
[http://dx.doi.org/10.1002/14651858.CD006378.pub2] [PMID: 22336816]
[21]
Barron M, Gartlon J, Dawson LA, Atkinson PJ, Pardon MC. A state of delirium: Deciphering the effect of inflammation on tau pathology in Alzheimer’s disease. Exp Gerontol 2017; 94: 103-7.
[http://dx.doi.org/10.1016/j.exger.2016.12.006] [PMID: 27979768]
[22]
Uddin MS, Al Mamun A, Kabir MT, et al. Nootropic and anti-Alzheimer’s actions of medicinal plants: molecular insight into therapeutic potential to alleviate alzheimer’s neuropathology. Mol Neurobiol 2019; 56(7): 4925-44.
[http://dx.doi.org/10.1007/s12035-018-1420-2] [PMID: 30414087]
[23]
Uddin MS, Uddin GMS, Begum MM, et al. Inspection of phytochemical content and in vitro antioxidant profile of Gnaphalium Luteoalbum L.: An unexplored phytomedicine. J Pharm Nutr Sci 2017; 7: 136-46.
[http://dx.doi.org/10.6000/1927-5951.2017.07.03.10]
[24]
Rahman A, Haque A, Uddin MS, et al. In vitro screening for antioxidant and anticholinesterase effects of uvaria littoralis blume: a nootropic phytotherapeutic remedy. J Intellect Disabil - Diagnosis Treat 2017; p. 5.
[25]
Essa MM, Vijayan RK, Castellano-Gonzalez G, Memon MA, Braidy N, Guillemin GJ. Neuroprotective effect of natural products against Alzheimer’s disease. Neurochem Res 2012; 37(9): 1829-42.
[http://dx.doi.org/10.1007/s11064-012-0799-9] [PMID: 22614926]
[26]
Kim J, Lee HJ, Lee KW. Naturally occurring phytochemicals for the prevention of Alzheimer’s disease. J Neurochem 2010; 112(6): 1415-30.
[http://dx.doi.org/10.1111/j.1471-4159.2009.06562.x] [PMID: 20050972]
[27]
Morales I, Guzman-Martinez L, Cerda-Troncoso C. FarÃas GA, Maccioni RB. Neuroinflammation in the pathogenesis of alzheimerâ disease. a rational framework for the search of novel therapeutic approaches. Front Cell Neurosci 2014; 8: 112.
[http://dx.doi.org/10.3389/fncel.2014.00112] [PMID: 24795567]
[28]
Uddin MS, Hossain MF, Al Mamun A, et al. Exploring the multimodal role of phytochemicals in the modulation of cellular signaling pathways to combat age-related neurodegeneration. Sci Total Environ 2020; 725138313
[http://dx.doi.org/10.1016/j.scitotenv.2020.138313]
[29]
Matsuura HN, Fett-Neto AG. Plant alkaloids: Main features, toxicity, and mechanisms of action. Dordrecht: Springer 2017; pp. 243-61.
[30]
Amirkia V, Heinrich M. Alkaloids as drug leads - a predictive structural and biodiversity-based analysis. Phytochem Lett 2014; 10: xlviii-53.
[http://dx.doi.org/10.1016/j.phytol.2014.06.015]
[31]
Ng YP, Or TCT, Ip NY. Plant alkaloids as drug leads for Alzheimer’s disease. Neurochem Int 2015; 89: 260-70.
[http://dx.doi.org/10.1016/j.neuint.2015.07.018] [PMID: 26220901]
[32]
Cordell GA. The alkaloids chemistry and biology. Academic Press 2006; p. 63.
[33]
de Almeida WAM, de Andrade JP, Chacon DS, et al. Isoquinoline alkaloids reduce beta-amyloid peptide toxicity in Caenorhabditis elegans. Nat Prod Res 2020; 1-5.
[http://dx.doi.org/10.1080/14786419.2020.1727471] [PMID: 32067490]
[34]
Martins N. Ferreira, I.C.F.R. An upcoming approach to Alzheimer’s disease: ethnopharmacological potential of plant bioactive molecules. Curr Med Chem 2020; 27(26): 4344-71.
[http://dx.doi.org/10.2174/0929867327666200219120806]
[35]
Querfurth HW, LaFerla FM. Alzheimer’s disease. N Engl J Med 2010; 362(4): 329-44.
[http://dx.doi.org/10.1056/NEJMra0909142] [PMID: 20107219]
[36]
Kabir MT, Uddin MS, Setu JR, Ashraf GM, Bin-Jumah MN, Abdel-Daim MM. Exploring the role of PSEN mutations in the pathogenesis of Alzheimer’s disease. Neurotox Res 2020.
[http://dx.doi.org/10.1007/s12640-020-00232-x.]]
[37]
Edler MK, Sherwood CC, Meindl RS, et al. Aged chimpanzees exhibit pathologic hallmarks of Alzheimer’s disease. Neurobiol Aging 2017; 59: 107-20.
[http://dx.doi.org/10.1016/j.neurobiolaging.2017.07.006] [PMID: 28888720]
[38]
Uddin MS, Upaganlawar AB. Oxidative stress and antioxidant defense: biomedical value in health and diseases. USA: Nova Science Publishers 2019.
[39]
Uddin MS, Kabir MT. Emerging signal regulating potential of genistein against Alzheimer’s disease: a promising molecule of interest. Front Cell Dev Biol 2019; 7: 197.
[http://dx.doi.org/10.3389/fcell.2019.00197] [PMID: 31620438]
[40]
LaFerla FM, Green KN, Oddo S. Intracellular amyloid-β in Alzheimer’s disease. Nat Rev Neurosci 2007; 8(7): 499-509.
[http://dx.doi.org/10.1038/nrn2168] [PMID: 17551515]
[41]
Cimini S, Sclip A, Mancini S, et al. The cell-permeable Aβ1-6A2VTAT(D) peptide reverts synaptopathy induced by Aβ1-42wt. Neurobiol Dis 2016; 89: 101-11.
[http://dx.doi.org/10.1016/j.nbd.2015.12.013] [PMID: 26721320]
[42]
Castillo WO, Aristizabal-Pachon AF. Galantamine protects against beta amyloid peptide-induced DNA damage in a model for Alzheimer’s disease. Neural Regen Res 2017; 12(6): 916-7.
[http://dx.doi.org/10.4103/1673-5374.208572] [PMID: 28761423]
[43]
Uddin MS, Stachowiak A, Mamun AA, et al. Autophagy and Alzheimer’s disease: from molecular mechanisms to therapeutic implications Front Aging Neurosci 2018. 10: 04.
[http://dx.doi.org/10.3389/fnagi.2018.00004] [PMID: 29441009]
[44]
Kitazawa M, Medeiros R, Laferla FM. Transgenic mouse models of Alzheimer disease: developing a better model as a tool for therapeutic interventions. Curr Pharm Des 2012; 18(8): 1131-47.
[http://dx.doi.org/10.2174/138161212799315786] [PMID: 22288400]
[45]
Uddin MS, Kabir MT, Al Mamun A, Abdel-Daim MM, Barreto GE, Ashraf GM. APOE and Alzheimer’s disease: Evidence mounts that targeting APOE4 may combat Alzheimer’s pathogenesis. Mol Neurobiol 2019; 56(4): 2450-65.
[http://dx.doi.org/10.1007/s12035-018-1237-z] [PMID: 30032423]
[46]
Uddin MS, Kabir MT, Tewari D, Mathew B, Aleya L. Emerging signal regulating potential of small molecule biflavonoids to combat neuropathological insults of Alzheimer’s disease. Sci Total Environ 2020; 700134836
[http://dx.doi.org/10.1016/j.scitotenv.2019.134836] [PMID: 31704512]
[47]
Uddin MS, Kabir MT, Rahman MM, Mathew B, Shah MA, Ashraf GM. TV 3326 for Alzheimer’s dementia: A novel multimodal che and MAO inhibitors to mitigate Alzheimer’s‐like neuropathology. J Pharm Pharmacol 2020; 72(8): 1001-12.
[48]
Uddin MS, Kabir MT, Niaz K, et al. Molecular insight into the therapeutic promise of flavonoids against Alzheimer’s disease. Molecules 2020; 25(6): 1267.
[http://dx.doi.org/10.3390/molecules25061267] [PMID: 32168835]
[49]
Cummings J, Lee G, Mortsdorf T, Ritter A, Zhong K. Alzheimer’s disease drug development pipeline: 2017. Alzheimers Dement (N Y) 2017; 3(3): 367-84.
[http://dx.doi.org/10.1016/j.trci.2017.05.002] [PMID: 29067343]
[50]
Uddin MS, Tewari D, Mamun AA, et al. Circadian and sleep dysfunction in Alzheimer’s disease. Ageing Res Rev 2020; 60101046
[http://dx.doi.org/10.1016/j.arr.2020.101046] [PMID: 32171783]
[51]
Alonso A, Zaidi T, Novak M, Grundke-Iqbal I, Iqbal K. Hyperphosphorylation induces self-assembly of τ into tangles of paired helical filaments/straight filaments. Proc Natl Acad Sci USA 2001; 98(12): 6923-8.
[http://dx.doi.org/10.1073/pnas.121119298] [PMID: 11381127]
[52]
Mamun AA, Uddin MS, Mathew B, Ashraf GM. Toxic tau: structural origins of tau aggregation in Alzheimer’s disease. Neural Regen Res 2020; 15(8): 1417-20.
[http://dx.doi.org/10.4103/1673-5374.274329] [PMID: 31997800]
[53]
Hensley K. Neuroinflammation in Alzheimer’s disease: mechanisms, pathologic consequences, and potential for therapeutic manipulation. J Alzheimers Dis 2010; 21(1): 1-14.
[http://dx.doi.org/10.3233/JAD-2010-1414] [PMID: 20182045]
[54]
Heneka MT, Carson MJ, El Khoury J, et al. Neuroinflammation in Alzheimer’s disease. Lancet Neurol 2015; 14(4): 388-405.
[http://dx.doi.org/10.1016/S1474-4422(15)70016-5] [PMID: 25792098]
[55]
Griffin WST, Stanley LC, Ling C, et al. Brain interleukin 1 and S-100 immunoreactivity are elevated in Down syndrome and Alzheimer disease. Proc Natl Acad Sci USA 1989; 86(19): 7611-5.
[http://dx.doi.org/10.1073/pnas.86.19.7611] [PMID: 2529544]
[56]
Rogers J, Luber-Narod J, Styren SD, Civin WH. Expression of immune system-associated antigens by cells of the human central nervous system: relationship to the pathology of Alzheimer’s disease. Neurobiol Aging 1988; 9(4): 339-49.
[http://dx.doi.org/10.1016/S0197-4580(88)80079-4] [PMID: 3263583]
[57]
Wyss-Coray T, Yan F, Lin AHT, et al. Prominent neurodegeneration and increased plaque formation in complement-inhibited Alzheimer’s mice. Proc Natl Acad Sci USA 2002; 99(16): 10837-42.
[http://dx.doi.org/10.1073/pnas.162350199] [PMID: 12119423]
[58]
Breitner JCS, Gau BA, Welsh KA, et al. Inverse association of anti-inflammatory treatments and Alzheimer’s disease: initial results of a co-twin control study. Neurology 1994; 44(2): 227-32.
[http://dx.doi.org/10.1212/WNL.44.2.227] [PMID: 8309563]
[59]
Rich JB, Rasmusson DX, Folstein MF, Carson KA, Kawas C, Brandt J. Nonsteroidal anti-inflammatory drugs in Alzheimer’s disease. Neurology 1995; 45(1): 51-5.
[http://dx.doi.org/10.1212/WNL.45.1.51] [PMID: 7824134]
[60]
McGeer PL, McGeer EG. NSAIDs and Alzheimer disease: epidemiological, animal model and clinical studies. Neurobiol Aging 2007; 28(5): 639-47.
[http://dx.doi.org/10.1016/j.neurobiolaging.2006.03.013] [PMID: 16697488]
[61]
Miguel-Álvarez M, Santos-Lozano A, Sanchis-Gomar F, et al. Non-steroidal anti-inflammatory drugs as a treatment for Alzheimer’s disease: a systematic review and meta-analysis of treatment effect. Drugs Aging 2015; 32(2): 139-47.
[http://dx.doi.org/10.1007/s40266-015-0239-z] [PMID: 25644018]
[62]
McGeer PL, Rogers J. Anti-inflammatory agents as a therapeutic approach to Alzheimer’s disease. Neurology 1992; 42(2): 447-9.
[http://dx.doi.org/10.1212/WNL.42.2.447] [PMID: 1736183]
[63]
Zotova E, Nicoll JA, Kalaria R, Holmes C, Boche D. Inflammation in Alzheimer’s disease: relevance to pathogenesis and therapy. Alzheimers Res Ther 2010; 2(1): 1.
[http://dx.doi.org/10.1186/alzrt24] [PMID: 20122289]
[64]
Kim YS, Joh TH. Microglia, major player in the brain inflammation: their roles in the pathogenesis of Parkinson’s disease. Exp Mol Med 2006; 38(4): 333-47.
[http://dx.doi.org/10.1038/emm.2006.40] [PMID: 16953112]
[65]
Uddin MS, Kabir MT, Mamun AA, et al. Pharmacological approaches to mitigate neuroinflammation in Alzheimer’s disease. Int Immunopharmacol 2020; 84106479
[http://dx.doi.org/10.1016/j.intimp.2020.106479] [PMID: 32353686]
[66]
Goldgaber D, Harris HW, Hla T, et al. Interleukin 1 regulates synthesis of amyloid β-protein precursor mRNA in human endothelial cells. Proc Natl Acad Sci USA 1989; 86(19): 7606-10.
[http://dx.doi.org/10.1073/pnas.86.19.7606] [PMID: 2508093]
[67]
Plassman BL, Havlik RJ, Steffens DC, et al. Documented head injury in early adulthood and risk of Alzheimer’s disease and other dementias. Neurology 2000; 55(8): 1158-66.
[http://dx.doi.org/10.1212/WNL.55.8.1158] [PMID: 11071494]
[68]
Quintanilla RA, Orellana DI, González-Billault C, Maccioni RB. Interleukin-6 induces Alzheimer-type phosphorylation of tau protein by deregulating the cdk5/p35 pathway. Exp Cell Res 2004; 295(1): 245-57.
[http://dx.doi.org/10.1016/j.yexcr.2004.01.002] [PMID: 15051507]
[69]
Cherry JD, Olschowka JA, O’Banion MK. Neuroinflammation and M2 microglia: the good, the bad, and the inflamed. J Neuroinflammation 2014; 11: 98.
[http://dx.doi.org/10.1186/1742-2094-11-98] [PMID: 24889886]
[70]
Streit WJ. Microglial activation and neuroinflammation in Alzheimer’s disease: a critical examination of recent history. Front Aging Neurosci 2010; 2: 22.
[http://dx.doi.org/10.3389/fnagi.2010.00022] [PMID: 20577641]
[71]
Bolmont T, Haiss F, Eicke D, et al. Dynamics of the microglial/amyloid interaction indicate a role in plaque maintenance. J Neurosci 2008; 28(16): 4283-92.
[http://dx.doi.org/10.1523/JNEUROSCI.4814-07.2008] [PMID: 18417708]
[72]
Baik SH, Kang S, Son SM, Mook-Jung I. Microglia contributes to plaque growth by cell death due to uptake of amyloid β in the brain of Alzheimer’s disease mouse model. Glia 2016; 64(12): 2274-90.
[http://dx.doi.org/10.1002/glia.23074] [PMID: 27658617]
[73]
Stalder M, Phinney A, Probst A, Sommer B, Staufenbiel M, Jucker M. Association of microglia with amyloid plaques in brains of APP23 transgenic mice. Am J Pathol 1999; 154(6): 1673-84.
[http://dx.doi.org/10.1016/S0002-9440(10)65423-5] [PMID: 10362792]
[74]
Bard F, Cannon C, Barbour R, et al. Peripherally administered antibodies against amyloid β-peptide enter the central nervous system and reduce pathology in a mouse model of Alzheimer disease. Nat Med 2000; 6(8): 916-9.
[http://dx.doi.org/10.1038/78682] [PMID: 10932230]
[75]
Simard AR, Soulet D, Gowing G, Julien J-P, Rivest S. Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer’s disease. Neuron 2006; 49(4): 489-502.
[http://dx.doi.org/10.1016/j.neuron.2006.01.022] [PMID: 16476660]
[76]
Tamboli IY, Barth E, Christian L, et al. Statins promote the degradation of extracellular amyloid β-peptide by microglia via stimulation of exosome-associated insulin-degrading enzyme (IDE) secretion. J Biol Chem 2010; 285(48): 37405-14.
[http://dx.doi.org/10.1074/jbc.M110.149468] [PMID: 20876579]
[77]
Yuyama K, Sun H, Mitsutake S, Igarashi Y. Sphingolipid-modulated exosome secretion promotes clearance of amyloid-β by microglia. J Biol Chem 2012; 287(14): 10977-89.
[http://dx.doi.org/10.1074/jbc.M111.324616] [PMID: 22303002]
[78]
Hickman SE, Allison EK, El Khoury J. Microglial dysfunction and defective β-amyloid clearance pathways in aging Alzheimer’s disease mice. J Neurosci 2008; 28(33): 8354-60.
[http://dx.doi.org/10.1523/JNEUROSCI.0616-08.2008] [PMID: 18701698]
[79]
Meda L, Cassatella MA, Szendrei GI, et al. Activation of microglial cells by β-amyloid protein and interferon-γ. Nature 1995; 374(6523): 647-50.
[http://dx.doi.org/10.1038/374647a0] [PMID: 7715705]
[80]
Sheng JG, Zhou XQ, Mrak RE, Griffin WST. Progressive neuronal injury associated with amyloid plaque formation in Alzheimer disease. J Neuropathol Exp Neurol 1998; 57(7): 714-7.
[http://dx.doi.org/10.1097/00005072-199807000-00008] [PMID: 9690675]
[81]
Krabbe G, Halle A, Matyash V, et al. Functional impairment of microglia coincides with Beta-amyloid deposition in mice with Alzheimer-like pathology. PLoS One 2013; 8(4)e60921
[http://dx.doi.org/10.1371/journal.pone.0060921] [PMID: 23577177]
[82]
Michelucci A, Heurtaux T, Grandbarbe L, Morga E, Heuschling P. Characterization of the microglial phenotype under specific pro-inflammatory and anti-inflammatory conditions: Effects of oligomeric and fibrillar amyloid-β. J Neuroimmunol 2009; 210(1-2): 3-12.
[http://dx.doi.org/10.1016/j.jneuroim.2009.02.003] [PMID: 19269040]
[83]
Bhaskar K, Maphis N, Xu G, et al. Microglial derived tumor necrosis factor-α drives Alzheimer’s disease-related neuronal cell cycle events. Neurobiol Dis 2014; 62: 273-85.
[http://dx.doi.org/10.1016/j.nbd.2013.10.007] [PMID: 24141019]
[84]
Smith JA, Das A, Ray SK, Banik NL. Role of pro-inflammatory cytokines released from microglia in neurodegenerative diseases. Brain Res Bull 2012; 87(1): 10-20.
[http://dx.doi.org/10.1016/j.brainresbull.2011.10.004] [PMID: 22024597]
[85]
Yates SL, Burgess LH, Kocsis-Angle J, et al. Amyloid β and amylin fibrils induce increases in proinflammatory cytokine and chemokine production by THP-1 cells and murine microglia. J Neurochem 2000; 74(3): 1017-25.
[http://dx.doi.org/10.1046/j.1471-4159.2000.0741017.x] [PMID: 10693932]
[86]
Wisniewski HM, Moretz RC, Lossinsky AS. Evidence for induction of localized amyloid deposits and neuritic plaques by an infectious agent. Ann Neurol 1981; 10(6): 517-22.
[http://dx.doi.org/10.1002/ana.410100605] [PMID: 7198888]
[87]
Jay TR, Miller CM, Cheng PJ, et al. TREM2 deficiency eliminates TREM2+ inflammatory macrophages and ameliorates pathology in Alzheimer’s disease mouse models. J Exp Med 2015; 212(3): 287-95.
[http://dx.doi.org/10.1084/jem.20142322] [PMID: 25732305]
[88]
Bemiller SM, McCray TJ, Allan K, et al. TREM2 deficiency exacerbates tau pathology through dysregulated kinase signaling in a mouse model of tauopathy. Mol Neurodegener 2017; 12(1): 74.
[http://dx.doi.org/10.1186/s13024-017-0216-6] [PMID: 29037207]
[89]
Wang Y, Cella M, Mallinson K, et al. TREM2 lipid sensing sustains the microglial response in an Alzheimer’s disease model. Cell 2015; 160(6): 1061-71.
[http://dx.doi.org/10.1016/j.cell.2015.01.049] [PMID: 25728668]
[90]
Savage JC, Jay T, Goduni E, et al. Nuclear receptors license phagocytosis by trem2+ myeloid cells in mouse models of Alzheimer’s disease. J Neurosci 2015; 35(16): 6532-43.
[http://dx.doi.org/10.1523/JNEUROSCI.4586-14.2015] [PMID: 25904803]
[91]
Guerreiro R, Wojtas A, Bras J, et al. Alzheimer Genetic Analysis Group. TREM2 variants in Alzheimer’s disease. N Engl J Med 2013; 368(2): 117-27.
[http://dx.doi.org/10.1056/NEJMoa1211851] [PMID: 23150934]
[92]
Hickman SE, El Khoury J. TREM2 and the neuroimmunology of Alzheimer’s disease. Biochem Pharmacol 2014; 88(4): 495-8.
[http://dx.doi.org/10.1016/j.bcp.2013.11.021] [PMID: 24355566]
[93]
Jin SC, Carrasquillo MM, Benitez BA, et al. TREM2 is associated with increased risk for Alzheimer’s disease in African Americans. Mol Neurodegener 2015; 10: 19.
[http://dx.doi.org/10.1186/s13024-015-0016-9] [PMID: 25886450]
[94]
Jonsson T, Stefansson H, Steinberg S, et al. Variant of TREM2 associated with the risk of Alzheimer’s disease. N Engl J Med 2013; 368(2): 107-16.
[http://dx.doi.org/10.1056/NEJMoa1211103] [PMID: 23150908]
[95]
Cortes N, Sabogal-Guaqueta AM, Cardona-Gomez GP, Osorio E. Neuroprotection and improvement of the histopathological and behavioral impairments in a murine Alzheimer’s model treated with Zephyranthes carinata alkaloids. Biomed Pharmacother 2019; 110: 482-92.
[http://dx.doi.org/10.1016/j.biopha.2018.12.013] [PMID: 30530228]
[96]
Serseg T, Benarous K, Lamrani M, Yousfi M. Lepidine B from lepidium sativum seeds as multi-functional anti-alzheimer’s disease agent: in vitro and in silico studies. In: Curr Comput Aided Drug Des. 2020; 16.
[97]
Valencia-Lozano E, Cabrera-Ponce JL, Gómez-Lim MA, Ibarra JE. Development of an efficient protocol to obtain transgenic coffee, Coffea arabica L., expressing the Cry10Aa toxin of Bacillus thuringiensis. Int J Mol Sci 2019; 20(21): 20.
[http://dx.doi.org/10.3390/ijms20215334] [PMID: 31717779]
[98]
Uddin MS, Abu Sufian M, Hossain MF, et al. Neuropsychological effects of caffeine: is caffeine addictive? J Psychol Psychother 2017; 07: 1-12.
[http://dx.doi.org/10.4172/2161-0487.1000295]
[99]
Johnson-Kozlow M, Kritz-Silverstein D, Barrett-Connor E, Morton D. Coffee consumption and cognitive function among older adults. Am J Epidemiol 2002; 156(9): 842-50.
[http://dx.doi.org/10.1093/aje/kwf119] [PMID: 12397002]
[100]
Ritchie K, Carrière I, de Mendonça A, et al. The neuroprotective effects of caffeine: a prospective population study (the Three City Study). Neurology 2007; 69(6): 536-45.
[http://dx.doi.org/10.1212/01.wnl.0000266670.35219.0c] [PMID: 17679672]
[101]
van Gelder BM, Buijsse B, Tijhuis M, et al. Coffee consumption is inversely associated with cognitive decline in elderly European men: the FINE Study. Eur J Clin Nutr 2007; 61(2): 226-32.
[http://dx.doi.org/10.1038/sj.ejcn.1602495] [PMID: 16929246]
[102]
Arab L, Khan F, Lam H. Epidemiologic evidence of a relationship between tea, coffee, or caffeine consumption and cognitive decline. Adv Nutr 2013; 4(1): 115-22.
[http://dx.doi.org/10.3945/an.112.002717] [PMID: 23319129]
[103]
Cao C, Cirrito JR, Lin X, et al. Caffeine suppresses amyloid-β levels in plasma and brain of Alzheimer’s disease transgenic mice. J Alzheimers Dis 2009; 17(3): 681-97.
[http://dx.doi.org/10.3233/JAD-2009-1071] [PMID: 19581723]
[104]
Laurent C, Eddarkaoui S, Derisbourg M, et al. Beneficial effects of caffeine in a transgenic model of Alzheimer’s disease-like tau pathology. Neurobiol Aging 2014; 35(9): 2079-90.
[http://dx.doi.org/10.1016/j.neurobiolaging.2014.03.027] [PMID: 24780254]
[105]
Ujiie M, Dickstein DL, Carlow DA, Jefferies WA. Blood-brain barrier permeability precedes senile plaque formation in an Alzheimer disease model. Microcirculation 2003; 10(6): 463-70.
[PMID: 14745459]
[106]
Chen X, Gawryluk JW, Wagener JF, Ghribi O, Geiger JD. Caffeine blocks disruption of blood brain barrier in a rabbit model of Alzheimer’s disease. J Neuroinflammation 2008; 5: 12.
[http://dx.doi.org/10.1186/1742-2094-5-12] [PMID: 18387175]
[107]
Harilal S, Jose J, Parambi DJG, et al. Revisiting the Blood-brain barrier: A hard nut to crack in the transportation of drug Molecules. Brain Res Bull 2020; 160: 121-40.
[http://dx.doi.org/10.1016/j.brainresbull.2020.03.018] [PMID: 32315731]
[108]
Kuo YM, Kokjohn TA, Watson MD, et al. Elevated abeta42 in skeletal muscle of Alzheimer disease patients suggests peripheral alterations of AbetaPP metabolism. Am J Pathol 2000; 156(3): 797-805.
[http://dx.doi.org/10.1016/S0002-9440(10)64947-4] [PMID: 10702395]
[109]
Chen X, Ghribi O, Geiger JD. Caffeine protects against disruptions of the blood-brain barrier in animal models of Alzheimer’s and Parkinson’s diseases. J Alzheimers Dis 2010; 20.
[http://dx.doi.org/10.3233/JAD-2010-1376]
[110]
Farkas IG, Czigner A, Farkas E, et al. Beta-amyloid peptide-induced blood-brain barrier disruption facilitates T-cell entry into the rat brain. Acta Histochem 2003; 105(2): 115-25.
[http://dx.doi.org/10.1078/0065-1281-00696] [PMID: 12831163]
[111]
Ullah F, Ali T, Ullah N, Kim MO. Caffeine prevents d-galactose-induced cognitive deficits, oxidative stress, neuroinflammation and neurodegeneration in the adult rat brain. Neurochem Int 2015; 90: 114-24.
[http://dx.doi.org/10.1016/j.neuint.2015.07.001] [PMID: 26209154]
[112]
Dall’Igna OP, Fett P, Gomes MW, Souza DO, Cunha RA, Lara DR. Caffeine and adenosine A(2a) receptor antagonists prevent β-amyloid (25-35)-induced cognitive deficits in mice. Exp Neurol 2007; 203(1): 241-5.
[http://dx.doi.org/10.1016/j.expneurol.2006.08.008] [PMID: 17007839]
[113]
Canas PM, Porciúncula LO, Cunha GMA, et al. Adenosine A2A receptor blockade prevents synaptotoxicity and memory dysfunction caused by β-amyloid peptides via p38 mitogen-activated protein kinase pathway. J Neurosci 2009; 29(47): 14741-51.
[http://dx.doi.org/10.1523/JNEUROSCI.3728-09.2009] [PMID: 19940169]
[114]
Arendash GW, Cao C. Caffeine and coffee as therapeutics against Alzheimer’s disease. J Alzheimers Dis 2010; 20.
[http://dx.doi.org/10.3233/JAD-2010-091249]
[115]
Zhang Q, Piao XL, Piao XS, Lu T, Wang D, Kim SW. Preventive effect of Coptis chinensis and berberine on intestinal injury in rats challenged with lipopolysaccharides. Food Chem Toxicol 2011; 49(1): 61-9.
[http://dx.doi.org/10.1016/j.fct.2010.09.032] [PMID: 20932871]
[116]
Asai M, Iwata N, Yoshikawa A, et al. Berberine alters the processing of Alzheimer’s amyloid precursor protein to decrease Abeta secretion. Biochem Biophys Res Commun 2007; 352(2): 498-502.
[http://dx.doi.org/10.1016/j.bbrc.2006.11.043] [PMID: 17125739]
[117]
Jia L, Liu J, Song Z, et al. Berberine suppresses amyloid-beta-induced inflammatory response in microglia by inhibiting nuclear factor-kappaB and mitogen-activated protein kinase signalling pathways. J Pharm Pharmacol 2012; 64(10): 1510-21.
[http://dx.doi.org/10.1111/j.2042-7158.2012.01529.x] [PMID: 22943182]
[118]
Lee B, Sur B, Shim I, Lee H, Hahm DH. Phellodendron amurense and its major alkaloid compound, berberine ameliorates scopolamine-induced neuronal impairment and memory dysfunction in rats. Korean J Physiol Pharmacol 2012; 16(2): 79-89.
[http://dx.doi.org/10.4196/kjpp.2012.16.2.79] [PMID: 22563252]
[119]
Zhu XZ, Li X-Y, Liu J. Recent pharmacological studies on natural products in China. Eur J Pharmacol 2004; 500(1-3): 221-30.
[http://dx.doi.org/10.1016/j.ejphar.2004.07.027] [PMID: 15464035]
[120]
Zhang HY, Tang XC. Neuroprotective effects of huperzine A: new therapeutic targets for neurodegenerative disease. Trends Pharmacol Sci 2006; 27(12): 619-25.
[http://dx.doi.org/10.1016/j.tips.2006.10.004] [PMID: 17056129]
[121]
Ruan Q, Hu X, Ao H, et al. The neurovascular protective effects of huperzine A on D-galactose-induced inflammatory damage in the rat hippocampus. Gerontology 2014; 60(5): 424-39.
[http://dx.doi.org/10.1159/000358235] [PMID: 24969491]
[122]
Wang ZF, Tang LL, Yan H, Wang YJ, Tang XC. Effects of huperzine A on memory deficits and neurotrophic factors production after transient cerebral ischemia and reperfusion in mice. Pharmacol Biochem Behav 2006; 83(4): 603-11.
[http://dx.doi.org/10.1016/j.pbb.2006.03.027] [PMID: 16687166]
[123]
Tang L-L, Wang R, Tang X-C, Huperzine A. Huperzine A protects SHSY5Y neuroblastoma cells against oxidative stress damage via nerve growth factor production. Eur J Pharmacol 2005; 519(1-2): 9-15.
[http://dx.doi.org/10.1016/j.ejphar.2005.06.026] [PMID: 16111675]
[124]
Mao XY, Cao DF, Li X, et al. Huperzine a ameliorates cognitive deficits in streptozotocin-induced diabetic rats. Int J Mol Sci 2014; 15: 7667-83.
[http://dx.doi.org/10.3390/ijms15057667] [PMID: 24857910]
[125]
Wang ZF, Wang J, Zhang HY, Tang XC, Huperzine A. Huperzine A exhibits anti-inflammatory and neuroprotective effects in a rat model of transient focal cerebral ischemia. J Neurochem 2008; 106(4): 1594-603.
[http://dx.doi.org/10.1111/j.1471-4159.2008.05504.x] [PMID: 18513368]
[126]
Furukawa S, Yang L, Sameshima H. Galantamine, an acetylcholinesterase inhibitor, reduces brain damage induced by hypoxia-ischemia in newborn rats. Int J Dev Neurosci 2014; 37: 52-7.
[http://dx.doi.org/10.1016/j.ijdevneu.2014.06.011] [PMID: 24972037]
[127]
Jackisch R, Förster S, Kammerer M, et al. Inhibitory potency of choline esterase inhibitors on acetylcholine release and choline esterase activity in fresh specimens of human and rat neocortex. J Alzheimers Dis 2009; 16(3): 635-47.
[http://dx.doi.org/10.3233/JAD-2009-1008] [PMID: 19276558]
[128]
Liu X-J, Cao M-A, Li W-H, Shen C-S, Yan S-Q, Yuan C-S. Alkaloids from Sophora flavescens Aition. Fitoterapia 2010; 81(6): 524-7.
[http://dx.doi.org/10.1016/j.fitote.2010.01.008] [PMID: 20079811]
[129]
Shal B, Ding W, Ali H, Kim YS, Khan S. Anti-neuroinflammatory potential of natural products in attenuation of Alzheimer’s disease. Front Pharmacol 2018; 9: 548.
[http://dx.doi.org/10.3389/fphar.2018.00548] [PMID: 29896105]
[130]
Moghbel N, Ryu B, Ratsch A, Steadman KJ. Nicotine alkaloid levels, and nicotine to nornicotine conversion, in Australian Nicotiana species used as chewing tobacco. Heliyon 2017; 3(11)e00469
[http://dx.doi.org/10.1016/j.heliyon.2017.e00469] [PMID: 29264422]
[131]
Kuete V. Health effects of alkaloids from African medicinal plants Toxicological survey of African medicinal plants. Elsevier Inc. 2014; pp. 611-33.
[http://dx.doi.org/10.1016/B978-0-12-800018-2.00021-2]
[132]
Alkadhi AKH, Alzoubi K, Srivareerat MT, Tran T. Chronic psychosocial stress exacerbates impairment of synaptic plasticity in amyloid rat model of alzheimers disease: prevention by nicotine. Curr Alzheimer Res 2011; 8: 718-31.
[http://dx.doi.org/10.2174/156720511797633188] [PMID: 21453245]
[133]
Srivareerat M, Tran TT, Salim S, Aleisa AM, Alkadhi KA. Chronic nicotine restores normal Aβ levels and prevents short-term memory and E-LTP impairment in Aβ rat model of Alzheimer’s disease. Neurobiol Aging 2011; 32(5): 834-44.
[http://dx.doi.org/10.1016/j.neurobiolaging.2009.04.015] [PMID: 19464074]
[134]
Utsuki T, Shoaib M, Holloway HW, et al. Nicotine lowers the secretion of the Alzheimer’s amyloid β-protein precursor that contains amyloid β-peptide in rat. J Alzheimers Dis 2002; 4(5): 405-15.
[http://dx.doi.org/10.3233/JAD-2002-4507] [PMID: 12446972]
[135]
Liu Q, Zhang J, Zhu H, Qin C, Chen Q, Zhao B. Dissecting the signaling pathway of nicotine-mediated neuroprotection in a mouse Alzheimer disease model. FASEB J 2007; 21(1): 61-73.
[http://dx.doi.org/10.1096/fj.06-5841com] [PMID: 17135361]

Rights & Permissions Print Cite
© 2024 Bentham Science Publishers | Privacy Policy