Skip to main content
Key Specialties
Cardiology Diabetology Endocrinology Gastroenterology Geriatrics and Gerontology Gynecology and Obstetrics Hematology Infectious Disease Internal Medicine Nephrology Neurology Oncology Pediatrics Respiratory Medicine Rheumatology Surgery
Congress Coverage
2024 ACC Congress 2023 ESMO Congress 2023 EASD Congress 2023 ERS Congress 2023 ESC Congress 2023 EHA Congress 2023 ASCO Annual Meeting
Clinical Collections
Advances in Alzheimer’s

At a glance: The ONWARDS insulin icodec trials

A round-up of the ONWARDS phase 3 clinical trials evaluating the novel weekly insulin icodec in people with diabetes.
ADVANCED SEARCH
Log in
Top
BMC Neurology
Published in: BMC Neurology 1/2014

Open Access 01-12-2014 | Debate

Inverse correlation between Alzheimer’s disease and cancer: implication for a strong impact of regenerative propensity on neurodegeneration?

Authors: Jian-Ming Li, Chao Liu, Xia Hu, Yan Cai, Chao Ma, Xue-Gang Luo, Xiao-Xin Yan

Published in: BMC Neurology | Issue 1/2014

Login to get access

Abstract

Background

Recent studies have revealed an inverse epidemiological correlation between Alzheimer’s disease (AD) and cancer − patients with AD show a reduced risk of cancer, while cancer survivors are less likely to develop AD. These late discoveries in human subjects call for explorative studies to unlock the underlying biological mechanism, but also may shed new light on conceptual interrogation of the principal pathogenic players in AD etiology.

Discussion

Here we hypothesize that this negative correlation reflects a rebalance of biosynthetic propensity between body systems under the two disease statuses. In normal condition the body cellular systems are maintained homeostatically under a balanced cell degenerative vs. surviving/regenerative propensities, determined by biosynthetic resources for anabolic processing. AD pathogenesis involves neurodegeneration but also aberrant regenerative, or reactive anabolic, burden, while cancer development is driving by uncontrolled proliferation inherent with excessive anabolic activity. The aberrant neural regenerative propensity in AD pathogenesis and the uncontrolled cellular proliferative propensity in cancer pathogeneses can manifest as competitive processes, which could result in the inverse epidemiological correlation seen among the elderly.

Summary

The reduced prevalence of AD in cancer survivors may implicate a strong impact of aberrant neural regenerative burden in neurodegeneration. Further explorative studies into the inverse correlation between AD and cancer should include examinations of the proliferative propensity of tumor cells in AD models, and the development of AD-like neuropathology in cancer models as well as following anti-proliferative drug treatment.
Appendix
Available only for authorised users
Literature
1.
Fargo K, Bleiler L: Alzheimer’s association report. Alzheimers Dement. 2014, 10: e47-e92. 10.1016/j.jalz.2014.08.103.CrossRef
2.
Tong L, Ahn C, Symanski E, Lai D, Du XL: Temporal trends in the leading causes of death among a large national cohort of patients with colorectal cancer from 1975 to 2009 in the United States. Ann Epidemiol. 2014, 24: 411-417. 10.1016/j.annepidem.2014.01.005.CrossRefPubMed
3.
Roe CM, Behrens MI, Xiong C, Miller JP, Morris JC: Alzheimer disease and cancer. Neurology. 2005, 64: 895-898. 10.1212/01.WNL.0000152889.94785.51.CrossRefPubMed
4.
Roe CM, Fitzpatrick AL, Xiong C, Sieh W, Kuller L, Miller JP, Williams MM, Kopan R, Behrens MI, Morris JC: Cancer linked to Alzheimer disease but not vascular dementia. Neurology. 2010, 74: 106-112. 10.1212/WNL.0b013e3181c91873.CrossRefPubMedPubMedCentral
5.
Driver JA, Beiser A, Au R, Kreger BE, Splansky GL, Kurth T, Kiel DP, Lu KP, Seshadri S, Wolf PA: Inverse association between cancer and Alzheimer’s disease: results from the Framingham Heart Study. BMJ. 2012, 344: e1442-10.1136/bmj.e1442.CrossRefPubMedPubMedCentral
6.
Realmuto S, Cinturino A, Arnao V, Mazzola MA, Cupidi C, Aridon P, Ragonese P, Savettieri G, D’Amelio M: Tumor diagnosis preceding Alzheimer’s disease onset: is there a link between cancer and Alzheimer’s disease?. J Alzheimers Dis. 2012, 31: 177-182.PubMed
7.
Du XL, Cai Y, Symanski E: Association between chemotherapy and cognitive impairments in a large cohort of patients with colorectal cancer. Int J Oncol. 2013, 42: 2123-2133.PubMed
8.
Musicco M, Adorni F, Di Santo S, Prinelli F, Pettenati C, Caltagirone C, Palmer K, Russo A: Inverse occurrence of cancer and Alzheimer disease: a population-based incidence study. Neurology. 2013, 81: 322-328. 10.1212/WNL.0b013e31829c5ec1.CrossRefPubMed
9.
Ou SM, Lee YJ, Hu YW, Liu CJ, Chen TJ, Fuh JL, Wang SJ: Does Alzheimer’s disease protect against cancers? A nationwide population-based study. Neuroepidemiology. 2013, 40: 42-49. 10.1159/000341411.CrossRefPubMed
10.
White RS, Lipton RB, Hall CB, Steinerman JR: Nonmelanoma skin cancer is associated with reduced Alzheimer disease risk. Neurology. 2013, 80: 1966-1972. 10.1212/WNL.0b013e3182941990.CrossRefPubMedPubMedCentral
11.
Benito-León J1, Romero JP, Louis ED, Bermejo-Pareja F: Faster cognitive decline in elders without dementia and decreased risk of cancer mortality: NEDICES study. Neurology. 2014, 82: 1441-1448. 10.1212/WNL.0000000000000350.CrossRefPubMedPubMedCentral
12.
DeKosky ST, Scheff SW: Synapse loss in frontal cortex biopsies in Alzheimer’s disease: correlation with cognitive severity. Annals of Neurol. 1990, 27: 457-464. 10.1002/ana.410270502.CrossRef
13.
Terry RD, Masliah E, Salmon DP, Butters N, Deteresa R, Hill R, Hansen LA, Katzman R: Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Annals Neurol. 1991, 30: 572-580. 10.1002/ana.410300410.CrossRef
14.
Heinonen O, Soininen H, Sorvari H, Kosunen O, Paljarvi L, Koivisto E, Riekkinen PJ: Loss of synaptophysin-like immunoreactivity in the hippocampal formation is an early phenomenon in Alzheimer’s disease. Neuroscience. 1995, 64: 375-384. 10.1016/0306-4522(94)00422-2.CrossRefPubMed
15.
Masliah E, Mallory M, Alford M, DeTeresa R, Hansen LA, McKeel DW, Morris JC: Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease. Neurology. 2001, 56: 127-129. 10.1212/WNL.56.1.127.CrossRefPubMed
16.
Reddy PH, Mani G, Park BS, Jacques J, Murdoch G, Whetsell W, Kaye J, Manczak M: Differential loss of synaptic proteins in Alzheimer’s disease: implications for synaptic dysfunction. J Alzheimer’s Dis. 2005, 7: 103-117.
17.
Scheff SW, Price DA, Schmitt FA, Scheff MA, Mufson EJ: Synaptic loss in the inferior temporal gyrus in mild cognitive impairment and Alzheimer’s disease. J Alzheimer’s Dis. 2011, 24: 547-557.
18.
Berchtold NC, Coleman PD, Cribbs DH, Rogers J, Gillen DL, Cotman CW: Synaptic genes are extensively downregulated across multiple brain regions in normal human aging and Alzheimer’s disease. Neurobiol Aging. 2013, 34: 1653-1661. 10.1016/j.neurobiolaging.2012.11.024.CrossRefPubMed
19.
Berchtold NC, Sabbagh MN, Beach TG, Kim RC, Cribbs DH, Cotman CW: Brain gene expression patterns differentiate mild cognitive impairment from normal aged and Alzheimer’s disease. Neurobiol Aging. 2014, 35: 1961-1972. 10.1016/j.neurobiolaging.2014.03.031.CrossRefPubMedPubMedCentral
20.
Behrens MI, Lendon C, Roe CM: A common biological mechanism in cancer and Alzheimer’s disease?. Curr Alzheimer Res. 2009, 6: 196-204. 10.2174/156720509788486608.CrossRefPubMedPubMedCentral
21.
Cenini G, Sultana R, Memo M, Butterfield DA: Elevated levels of pro-apoptotic p53 and its oxidative modification by the lipid peroxidation product, HNE, in brain from subjects with amnestic mild cognitive impairment and Alzheimer’s disease. J Cell Mol Med. 2008, 12: 987-994. 10.1111/j.1582-4934.2008.00163.x.CrossRefPubMedPubMedCentral
22.
Hooper C, Meimaridou E, Tavassoli M, Melino G, Lovestone S, Killick R: p53 is upregulated in Alzheimer’s disease and induces tau phosphorylation in HEK293a cells. Neurosci Lett. 2007, 418: 34-37. 10.1016/j.neulet.2007.03.026.CrossRefPubMedPubMedCentral
23.
Sultana R, Boyd-Kimball D, Poon HF, Cai J, Pierce WM, Klein JB, Markesbery WR, Zhou XZ, Lu KP, Butterfield DA: Oxidative modification and down-regulation of Pin1 in Alzheimer’s disease hippocampus: a redox proteomics analysis. Neurobiol Aging. 2006, 27: 918-925. 10.1016/j.neurobiolaging.2005.05.005.CrossRefPubMed
24.
Wang S, Simon BP, Bennett DA, Schneider JA, Malter JS, Wang DS: The significance of Pin1 in the development of Alzheimer’s disease. J Alzheimers Dis. 2007, 11: 13-23.PubMed
25.
Geddes JW, Cotman CW: Plasticity in Alzheimer’s disease: too much or not enough?. Neurobiol Aging. 1991, 12: 330-333. 10.1016/0197-4580(91)90011-8. discussion 352-335CrossRefPubMed
26.
Arendt T: Alzheimer’s disease as a disorder of mechanisms underlying structural brain self-organization. Neuroscience. 2001, 102: 723-765. 10.1016/S0306-4522(00)00516-9.CrossRefPubMed
27.
Castellani RJ, Lee HG, Zhu X, Perry G, Smith MA: Alzheimer disease pathology as a host response. J Neuropathol Exp Neurol. 2008, 67: 523-531. 10.1097/NEN.0b013e318177eaf4.CrossRefPubMedPubMedCentral
28.
Williams C, Mehrian Shai R, Wu Y, Hsu YH, Sitzer T, Spann B, McCleary C, Mo Y, Miller CA: Transcriptome analysis of synaptoneurosomes identifies neuroplasticity genes overexpressed in incipient Alzheimer’s disease. PLoS One. 2009, 4: e4936-10.1371/journal.pone.0004936.CrossRefPubMedPubMedCentral
29.
Holohan KN, Lahiri DK, Schneider BP, Foroud T, Saykin AJ: Functional microRNAs in Alzheimer’s disease and cancer: differential regulation of common mechanisms and pathways. Front Genet. 2013, 3: 323-10.3389/fgene.2012.00323.CrossRefPubMedPubMedCentral
30.
Ferrer I, Marín C, Rey MJ, Ribalta T, Goutan E, Blanco R, Tolosa E, Martí E: BDNF and full-length and truncated TrkB expression in Alzheimer disease. implications in therapeutic strategies. J Neuropathol Exp Neurol. 1999, 58: 729-739. 10.1097/00005072-199907000-00007.CrossRefPubMed
31.
Zeng F, Lu JJ, Zhou XF, Wang YJ: Roles of p75NTR in the pathogenesis of Alzheimer’s disease: a novel therapeutic target. Biochem Pharmacol. 2011, 82: 1500-1509. 10.1016/j.bcp.2011.06.040.CrossRefPubMed
32.
Zeng F, Zou HQ, Zhou HD, Li J, Wang L, Cao HY, Yi X, Wang X, Liang CR, Wang YR, Zhang AQ, Tan XL, Peng KR, Zhang LL, Gao CY, Xu ZQ, Wen AQ, Lian Y, Zhou XF, Wang YJ: The relationship between single nucleotide polymorphisms of the NTRK2 gene and sporadic Alzheimer’s disease in the Chinese Han population. Neurosci Lett. 2013, 550: 55-59. 10.1016/j.neulet.2013.06.061.CrossRefPubMed
33.
Farfara D, Lifshitz V, Frenkel D: Neuroprotective and neurotoxic properties of glial cells in the pathogenesis of Alzheimer’s disease. J Cell Mol Med. 2008, 12: 762-780. 10.1111/j.1582-4934.2008.00314.x.CrossRefPubMedPubMedCentral
34.
35.
Avila-Muñoz E, Arias C: When astrocytes become harmful: functional and inflammatory responses that contribute to Alzheimer’s disease. Ageing Res Rev. 2014, 18C: 29-40. 10.1016/j.arr.2014.07.004.CrossRef
36.
Deng X, Li M, Ai W, He L, Lu D, Patrylo P, Cai H, Luo X, Li Z, Yan XX: Lipolysaccharide-induced neuroinflammation is associated with Alzheimer-like amyloidogenic axonal pathology and dendritic degeneration in rats. Adv Alzheimers Dis. 2014, 3: 78-93. 10.4236/aad.2014.32009.CrossRef
37.
Braak H, Braak E: Evolution of the neuropathology of Alzheimer’s disease. Acta Neurol Scand Suppl. 1996, 165: 3-12. 10.1111/j.1600-0404.1996.tb05866.x.CrossRefPubMed
38.
Soldano A, Hassan BA: Beyond pathology: APP, brain development and Alzheimer’s disease. Curr Opin Neurobiol. 2014, 27C: 61-67. 10.1016/j.conb.2014.02.003.CrossRef
39.
Shoji M, Hirai S, Yamaguchi H, Harigaya Y, Kawarabayashi T: Amyloid beta-protein precursor accumulates in dystrophic neurites of senile plaques in Alzheimer-type dementia. Brain Res. 1990, 512: 164-168. 10.1016/0006-8993(90)91187-L.CrossRefPubMed
40.
Cummings BJ, Su JH, Geddes JW, Van Nostrand WE, Wagner SL, Cunningham DD, Cotman CW: Aggregation of the amyloid precursor protein within degenerating neurons and dystrophic neurites in Alzheimer’s disease. Neuroscience. 1992, 48: 763-777. 10.1016/0306-4522(92)90265-4.CrossRefPubMed
41.
Cras P, Kawai M, Lowery D, Gonzalez-De Whitt P, Greenberg B, Perry G: Senile plaque neurites in Alzheimer disease accumulate amyloid precursor protein. Proc Natl Acad Sci U S A. 1991, 88: 7552-7556. 10.1073/pnas.88.17.7552.CrossRefPubMedPubMedCentral
42.
McGeer PL, Akiyama H, Kawamata T, Yamada T, Walker DG, Ishii T: Immunohistochemical localization of beta-amyloid precursor protein sequences in Alzheimer and normal brain tissue by light and electron microscopy. J Neurosci Res. 1992, 31: 428-442. 10.1002/jnr.490310305.CrossRefPubMed
43.
Zhang XM, Cai Y, Xiong K, Cai H, Luo XG, Feng JC, Clough RW, Struble RG, Patrylo PR, Yan XX: Beta-secretase-1 elevation in transgenic mouse models of Alzheimer’s disease is associated with synaptic/axonal pathology and amyloidogenesis: implications for neuritic plaque development. Eur J Neurosci. 2009, 30: 2271-2283. 10.1111/j.1460-9568.2009.07017.x.CrossRefPubMedPubMedCentral
44.
Cai Y, Xiong K, Zhang XM, Cai H, Luo XG, Feng JC, Clough RW, Struble RG, Patrylo PR, Chu Y, Kordower JH, Yan XX: ?-Secretase-1 elevation in aged monkey and Alzheimer’s disease human cerebral cortex occurs around the vasculature in partnership with multisystem axon terminal pathogenesis and ?-amyloid accumulation. Eur J Neurosci. 2010, 32: 1223-1238. 10.1111/j.1460-9568.2010.07376.x.CrossRefPubMedPubMedCentral
45.
Chui DH, Shirotani K, Tanahashi H, Akiyama H, Ozawa K, Kunishita T, Takahashi K, Makifuchi T, Tabira T: Both N-terminal and C-terminal fragments of presenilin 1 colocalize with neurofibrillary tangles in neurons and dystrophic neurites of senile plaques in Alzheimer’s disease. J Neurosci Res. 1998, 53: 99-106. 10.1002/(SICI)1097-4547(19980701)53:1<99::AID-JNR10>3.0.CO;2-Y.CrossRefPubMed
46.
Hendriks L, De Jonghe C, Lübke U, Woodrow S, Vanderhoeven I, Boons J, Cras P, Martin JJ, Van Broeckhoven C: Immunoreactivity of presenilin-1 and tau in Alzheimer’s disease brain. Exp Neurol. 1998, 149: 341-348. 10.1006/exnr.1997.6739.CrossRefPubMed
47.
Yang X, Handler M, Shen J: Role of presenilin-1 in murine neural development. Ann N Y Acad Sci. 2000, 920: 165-170. 10.1111/j.1749-6632.2000.tb06918.x.CrossRefPubMed
48.
Feng R, Rampon C, Tang YP, Shrom D, Jin J, Kyin M, Sopher B, Miller MW, Ware CB, Martin GM, Kim SH, Langdon RB, Sisodia SS, Tsien JZ: Deficient neurogenesis in forebrain-specific presenilin-1 knockout mice is associated with reduced clearance of hippocampal memory traces. Neuron. 2001, 32: 911-926. 10.1016/S0896-6273(01)00523-2.CrossRefPubMed
49.
Yan XX, Li T, Rominger CM, Prakash SR, Wong PC, Olson RE, Zaczek R, Li YW: Binding sites of gamma-secretase inhibitors in rodent brain: distribution, postnatal development, and effect of deafferentation. J Neurosci. 2004, 24: 2942-2952. 10.1523/JNEUROSCI.0092-04.2004.CrossRefPubMed
50.
Laird FM, Cai H, Savonenko AV, Farah MH, He K, Melnikova T, Wen H, Chiang HC, Xu G, Koliatsos VE, Borchelt DR, Price DL, Lee HK, Wong PC: BACE1, a major determinant of selective vulnerability of the brain to amyloid-beta amyloidogenesis, is essential for cognitive, emotional, and synaptic functions. J Neurosci. 2005, 25: 11693-11709. 10.1523/JNEUROSCI.2766-05.2005.CrossRefPubMedPubMedCentral
51.
Gadadhar A, Marr R, Lazarov O: Presenilin-1 regulates neural progenitor cell differentiation in the adult brain. J Neurosci. 2011, 31: 2615-2623. 10.1523/JNEUROSCI.4767-10.2011.CrossRefPubMedPubMedCentral
52.
Rajapaksha TW, Eimer WA, Bozza TC, Vassar R: The Alzheimer’s ?-secretase enzyme BACE1 is required for accurate axon guidance of olfactory sensory neurons and normal glomerulus formation in the olfactory bulb. Mol Neurodegener. 2011, 6: 88-10.1186/1750-1326-6-88.CrossRefPubMedPubMedCentral
53.
Cao L, Rickenbacher GT, Rodriguez S, Moulia TW, Albers MW: The precision of axon targeting of mouse olfactory sensory neurons requires the BACE1 protease. Sci Rep. 2012, 2: 231-PubMedPubMedCentral
54.
Yan XX, Ma C, Gai WP, Cai H, Luo XG: Can BACE1 inhibition mitigate early axonal pathology in neurological diseases?. J Alzheimers Dis. 2014, 38: 705-718.PubMedPubMedCentral
55.
Gentleman SM, Nash MJ, Sweeting CJ, Graham DI, Roberts GW: Beta-amyloid precursor protein (beta APP) as a marker for axonal injury after head injury. Neurosci Lett. 1993, 160: 139-144. 10.1016/0304-3940(93)90398-5.CrossRefPubMed
56.
Moussavi Nik SH, Wilson L, Newman M, Croft K, Mori TA, Musgrave I, Lardelli M: The BACE1-PSEN-A?PP regulatory axis has an ancient role in response to low oxygen/oxidative stress. J Alzheimers Dis. 2012, 28: 515-530.PubMed
57.
Li JM, Xue ZQ, Deng SH, Luo XG, Patrylo PR, Rose GW, Cai H, Cai Y, Yan XX: Amyloid plaque pathogenesis in 5XFAD mouse spinal cord: retrograde transneuronal modulation after peripheral nerve injury. Neurotox Res. 2013, 24: 1-14. 10.1007/s12640-012-9355-2.CrossRefPubMed
58.
Arendt T, Bullmann T: Neuronal plasticity in hibernation and the proposed role of the microtubule-associated protein tau as a “master switch” regulating synaptic gain in neuronal networks. Am J Physiol Regul Integr Comp Physiol. 2013, 305: R478-R489. 10.1152/ajpregu.00117.2013.CrossRefPubMed
59.
Miyasaka T, Sato S, Tatebayashi Y, Takashima A: Microtubule destruction induces tau liberation and its subsequent phosphorylation. FEBS Lett. 2010, 584: 3227-3232. 10.1016/j.febslet.2010.06.014.CrossRefPubMed
60.
Kuchibhotla KV, Wegmann S, Kopeikina KJ, Hawkes J, Rudinskiy N, Andermann ML, Spires-Jones TL, Bacskai BJ, Hyman BT: Neurofibrillary tangle-bearing neurons are functionally integrated in cortical circuits in vivo. Proc Natl Acad Sci U S A. 2014, 111: 510-514. 10.1073/pnas.1318807111.CrossRefPubMed
61.
Stoothoff WH, Johnson GV: Tau phosphorylation: physiological and pathological consequences. Biochim Biophys Acta. 2005, 1739: 280-297. 10.1016/j.bbadis.2004.06.017.CrossRefPubMed
62.
Raina AK1, Zhu X, Monteiro M, Takeda A, Smith MA: Abortive oncogeny and cell cycle-mediated events in Alzheimer disease. Prog Cell Cycle Res. 2000, 4: 235-242. 10.1007/978-1-4615-4253-7_20.CrossRefPubMed
63.
Arendt T: Cell cycle activation and aneuploid neurons in Alzheimer’s disease. Mol Neurobiol. 2012, 46: 125-135. 10.1007/s12035-012-8262-0.CrossRefPubMed
64.
Falandry C, Bonnefoy M, Freyer G, Gilson E: Biology of cancer and aging: a complex association with cellular senescence.J Clin Oncol 2014.,
65.
Suzuki H, Asakawa A, Amitani H, Nakamura N, Inui A: Cancer cachexia-pathophysiology and management. J Gastroenterol. 2013, 48: 574-594. 10.1007/s00535-013-0787-0.CrossRefPubMedPubMedCentral
66.
Demetrius LA, Simon DK: An inverse-Warburg effect and the origin of Alzheimer’s disease. Biogerontology. 2012, 13: 583-594. 10.1007/s10522-012-9403-6.CrossRefPubMed
67.
Driver JA: Inverse association between cancer and neurodegenerative disease: review of the epidemiologic and biological evidence. Biogerontology. 2014
68.
Tabares-Seisdedos R, Rubenstein JL: Inverse cancer comorbidity: a serendipitous opportunity to gain insight into CNS disorders. Nat Rev Neurosci. 2013, 14: 293-304. 10.1038/nrn3464.CrossRefPubMed
69.
Palsson-McDermott EM, O’Neill LA: The Warburg effect then and now: from cancer to inflammatory diseases. Bioessays. 2013, 35: 965-973. 10.1002/bies.201300084.CrossRefPubMed
70.
Costantini LC, Barr LJ, Vogel JL, Henderson ST: Hypometabolism as a therapeutic target in Alzheimer’s disease. BMC Neurosci. 2008, 9 (Suppl 2): S16-10.1186/1471-2202-9-S2-S16.CrossRefPubMedPubMedCentral
71.
Vander Heiden MG, Cantley LC, Thompson CB: Understanding the Warburg effect: the metabolic requirements of cell proliferation. Science. 2009, 324: 1029-1033. 10.1126/science.1160809.CrossRefPubMedPubMedCentral
72.
Agathocleous M, Harris WA: Metabolism in physiological cell proliferation and differentiation. Trends Cell Biol. 2013, 23: 484-492. 10.1016/j.tcb.2013.05.004.CrossRefPubMed
73.
Hayes CD, Dey D, Palavicini JP, Wang H, Patkar KA, Minond D, Nefzi A, Lakshmana MK: Striking reduction of amyloid plaque burden in an Alzheimer’s mouse model after chronic administration of carmustine. BMC Med. 2013, 11: 81-10.1186/1741-7015-11-81.CrossRefPubMedPubMedCentral
74.
Brunden KR, Trojanowski JQ, Smith AB 3rd, Lee VM, Ballatore C: Microtubule-stabilizing agents as potential therapeutics for neurodegenerative disease. Bioorg Med Chem. 2014, 22: 5040-5049. 10.1016/j.bmc.2013.12.046.CrossRefPubMed
Metadata
Title
Inverse correlation between Alzheimer’s disease and cancer: implication for a strong impact of regenerative propensity on neurodegeneration?
Authors
Jian-Ming Li
Chao Liu
Xia Hu
Yan Cai
Chao Ma
Xue-Gang Luo
Xiao-Xin Yan
Publication date
01-12-2014
Publisher
BioMed Central
Published in
BMC Neurology / Issue 1/2014
Electronic ISSN: 1471-2377
DOI
https://doi.org/10.1186/s12883-014-0211-2

Other articles of this Issue 1/2014

BMC Neurology 1/2014 Go to the issue

Research article

Deterioration after corticosteroids in CIDP may be associated with pure focal demyelination pattern

Research article

Changes of liver enzymes and bilirubin during ischemic stroke: mechanisms and possible significance

Research article

Card-placing test in amnestic mild cognitive impairment and its neural correlates

Research article

An immunoassay that distinguishes real neuromyelitis optica signals from a labeling detected in patients receiving natalizumab

Research article

Clinical significance of cerebrovascular complications in patients with acute infective endocarditis: a retrospective analysis of a 12-year single-center experience

Research article

Neuropsychological study of amyotrophic lateral sclerosis and parkinsonism-dementia complex in Kii peninsula, Japan