Skip to main content
SpringerLink
Log in

Lewy body pathology in Alzheimer’s disease

  • Published:
Journal of Molecular Neuroscience Aims and scope Submit manuscript

Abstract

Lewy bodies, the characteristic pathological lesion of substantia nigra neurons in Parkinson’s disease (PD), are frequently observed to accompany the amyloid plaque and neurofibrillary tangle pathology of Alzheimer’s disease (AD). However the typical anatomic distribution of Lewy bodies in AD is distinct from PD. The most common site of occurrence is the amygdala, where Lewy bodies are observed in approximately 60% of both sporadic and familial AD. Other common sites of occurrence include the periamygdaloid and entorhinal cortex, while neocortical and brainstem areas develop Lewy bodies in a lower percentage of cases. In contrast, dementia with Lewy bodies (DLB), defined by widespread neocortical and brainstem Lewy bodies but frequently accompanied by variable levels of AD-type pathology, represents the other end of a spectrum of pathology associated with dementia. The observation of Lewy bodies in familial AD cases suggests that like neurofibrillary tangles, the formation of Lewy bodies can be induced by the pathological state caused by Aβ-amyloid over-production. The role of Lewy body formation in the dysfunction and degeneration of neurons remains unclear. The protein α-synuclein appears to be an important structural component of Lewy bodies, an observation spurred by the discovery of point mutations in the α-synuclein gene linked to rare cases of autosomal dominant PD. Further investigation of α-synuclein and its relationship to pathological conditions promoting Lewy body formation in AD, PD, and DLB may yield further insight into pathogenesis of these diseases.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References

  • Abeliovich A., Schmitz Y., Farinas I., Choi-Lundberg D., Ho W. H., Castillo P. E., et al. (2000) Mice lacking alpha-synuclein display functional deficits in the nigrostriatal dopamine system. Neuron 25(1), 239–52.

    Article  PubMed  CAS  Google Scholar 

  • Arai K., Kato N., Kashiwado K., and Hattori T. (2000) Pure autonomic failure in association with human alpha-synucleinopathy. Neurosci. Lett. 296(2–3), 171–173.

    Article  PubMed  CAS  Google Scholar 

  • Arawaka S., Saito Y., Murayama S., and Mori H. (1998) Lewy body in neurodegeneration with brain iron accumulation type 1 is immunoreactive for alpha-synuclein. Neurology 51(3), 887–889.

    PubMed  CAS  Google Scholar 

  • Baba M., Nakajo S., Tu P. H., et al. (1998) Aggregation of alpha-synuclein in Lewy bodies of sporadic Parkinson’s disease and dementia with Lewy bodies. Am. J. Pathol. 152(4), 879–884.

    PubMed  CAS  Google Scholar 

  • Bayer T. A., Jakala P., Hartmann T., Egensperger R., Buslei R., Falkai P., and Beyreuther K. (1999) Neural expression profile of alpha-synuclein in developing human cortex. Neuroreport 10(13), 2799–2803.

    Article  PubMed  CAS  Google Scholar 

  • Bayer T. A., Jakala P., Hartmann T., Havas L., McLean C., Culvenor J. G., et al. (1999) Alpha-synuclein accumulates in Lewy bodies in Parkinson’s disease and dementia with Lewy bodies but not in Alzheimer’s disease beta-amyloid plaque cores. Neurosci. Lett. 266(3), 213–216.

    Article  PubMed  CAS  Google Scholar 

  • Betarbet R., Sherer T. B., Mackenzie G., Garcia-Osuna M., Panov A. V., and Greenamyre J. T. (2000) Chronic systemic pesticide exposure reproduces features of Parkinson’s disease. Nature Neurosci. 3(12), 1301–1306.

    Article  PubMed  CAS  Google Scholar 

  • Clayton D. F. and George J. M. (1998) The synucleins: a family of proteins involved in synaptic function, plasticity, neurodegeneration and disease. Trends Neurosci. 21(6), 249–254.

    Article  PubMed  CAS  Google Scholar 

  • Conway K. A., Harper J. D., and Lansbury P. T. (1998) Accelerated in vitro fibril formation by a mutant alpha-synuclein linked to early-onset Parkinson disease. Nat. Med. 4(11), 1318–1320.

    Article  PubMed  CAS  Google Scholar 

  • Culvenor J. G., McLean C. A., Cutt S., Campbell B. C., Maher F., Jakala P., et al. (1999) Non-Abeta component of Alzheimer’s disease amyloid (NAC) revisited. NAC and alpha-synuclein are not associated with Abeta amyloid. Am. J. Pathol. 155(4), 1173–1181.

    PubMed  CAS  Google Scholar 

  • da Costa C. A., Ancolio K., and Checler F. (2000) Wildtype but not Parkinson’s disease-related ala-53 → Thr mutant alpha -synuclein protects neuronal cells from apoptotic stimuli. J. Biol. Chem. 275(31), 24,065–24,069.

    Article  Google Scholar 

  • El-Agnaf O. M., Jakes R., Curran M. D., and Wallace A. (1998) Effects of the mutations Ala30 to Pro and Ala53 to Thr on the physical and morphological properties of alpha-synuclein protein implicated in Parkinson’s disease. FEBS Lett. 440(1–2), 67–70.

    Article  PubMed  CAS  Google Scholar 

  • Feany M. B. and Bender W. W. (2000) A Drosophila model of Parkinson’s disease. Nature 404(6776), 394–398.

    Article  PubMed  CAS  Google Scholar 

  • Forno L. S. (1996) Neuropathology of Parkinson’s disease. J. Neuropathol. Exp. Neurol. 55(3), 259–272.

    PubMed  CAS  Google Scholar 

  • Forstl H., Burns A., Luthert P., Cairns N., and Levy R. (1993) The Lewy-body variant of Alzheimer’s disease. Clinical and pathological findings. Br. J. Psychiatry 162, 385–392.

    Article  PubMed  CAS  Google Scholar 

  • Galasko D., Hansen L. A., Katzman R., Wiederholt W., Masliah E., Terry R., et al. (1994) Clinical-neuropathological correlations in Alzheimer’s disease and related dementias. Arch. Neurol. 51(9), 888–895.

    PubMed  CAS  Google Scholar 

  • Giasson B. I., Duda J. E., Murray I. V., Chen Q., Souza J. M., Hurtig H. I., et al. (2000) Oxidative damage linked to neurodegeneration by selective alpha-synuclein nitration in synucleinopathy lesions [In Process Citation]. Science 290(5493), 985–989.

    Article  PubMed  CAS  Google Scholar 

  • Giasson B. I., Uryu K., Trojanowski J. Q., and Lee V. M. (1999) Mutant and wild type human alpha-synucleins assemble into elongated filaments with distinct morphologies in vitro. J. Biol. Chem. 274(12), 7619–7622.

    Article  PubMed  CAS  Google Scholar 

  • Goedert M., Jakes R., Crowther R. A., Hasegawa M., Smith M. J., and Spillantini M. G. (1998) Intraneuronal filamentous tau protein and alpha-synuclein deposits in neurodegenerative diseases. Biochem. Soc. Trans. 26(3), 463–471.

    PubMed  CAS  Google Scholar 

  • Goldman J. E., Yen S. H., Chiu F. C., and Peress N. S. (1983) Lewy bodies of Parkinson’s disease contain neurofilament antigens. Science 221, 1082–1804.

    Article  PubMed  CAS  Google Scholar 

  • Gomez-Tortosa E., Ingraham A. O., Irizarry M. C., and Hyman B. T. (1998) Dementia with Lewy bodies. J. Am. Geriatr. Soc. 46(11), 1449–1458.

    PubMed  CAS  Google Scholar 

  • Gomez-Tortosa E., Irizarry M. C., Gomez-Isla T., and Hyman B. T. (2000) Clinical and neuropathological correlates of dementia with Lewy bodies. Ann. NY Acad. Sci. 920, 9–15.

    Article  PubMed  CAS  Google Scholar 

  • Hamilton R. L. (2000) Lewy bodies in Alzheimer’s disease: a neuropathological review of 145 cases using alpha-synuclein immunohistochemistry. Brain Pathol. 10(3), 378–384.

    Article  PubMed  CAS  Google Scholar 

  • Hansen L., Salmon D., Galasko D., Masliah E., Katzman R., DeTeresa R., et al. (1990) The Lewy body variant of Alzheimer’s disease: a clinical and pathologic entity. Neurology 40(1), 1–8.

    PubMed  CAS  Google Scholar 

  • Hansen L. A., Masliah E., Galasko D., and Terry R. D. (1993) Plaque-only Alzheimer disease is usually the lewy body variant, and vice versa. J. Neuropathol. Exp. Neurol. 52(6), 648–654.

    PubMed  CAS  Google Scholar 

  • Hartley D. M., Walsh D. M., Ye C. P., Diehl T., Vasquez S., Vassilev P. M., et al. (1999) Protofibrillar intermediates of amyloid beta-protein induce acute electrophysiological changes and progressive neurotoxicity in cortical neurons. J. Neurosci. 19(20), 8876–8884.

    PubMed  CAS  Google Scholar 

  • Heyman A., Fillenbaum G. G., Gearing M., Mirra S. S., Welsh-Bohmer K. A., Peterson B., and Pieper C. (1999) Comparison of Lewy body variant of Alzheimer’s disease with pure Alzheimer’s disease: Consortium to Establish a Registry for Alzheimer’s Disease, Part XIX. Neurology 52(9), 1839–1844.

    PubMed  CAS  Google Scholar 

  • Hsu L. J., Mallory M., Xia Y., Veinbergs I., Hashimoto M., Yoshimoto M., et al. (1998) Expression pattern of synucleins (non-Abeta component of Alzheimer’s disease amyloid precursor protein/alpha-synuclein) during murine brain development. J. Neurochem. 71(1), 338–344.

    Article  PubMed  CAS  Google Scholar 

  • Hsu L. J., Sagara Y., Arroyo A., Rockenstein E., Sisk A., Mallory M., et al. (2000) Alpha-synuclein promotes mitochondrial deficit and oxidative stress. Am. J. Pathol. 157(2), 401–410.

    PubMed  CAS  Google Scholar 

  • Hughes T. A., Ross H. F., Musa S., Bhattacherjee S., Nathan R. N., Mindham R. H., and Spokes E. G. (2000) A 10-year study of the incidence of and factors predicting dementia in Parkinson’s disease. Neurology 54(8), 1596–1602.

    PubMed  CAS  Google Scholar 

  • Hurtig H. I., Trojanowski J. Q., Galvin J., Ewbank D., Schmidt M. L., Lee V. M., et al. (2000) Alpha-synuclein cortical Lewy bodies correlate with dementia in Parkinson’s disease. Neurology 54(10), 1916–1921.

    PubMed  CAS  Google Scholar 

  • Ii K., Ito H., Tanaka K., and Hirano A. (1997) Immunocytochemical co-localization of the proteasome in ubiquitinated structures in neurodegenerative diseases and the elderly. J. Neuropathol. Exp. Neurol. 56(2), 125–131.

    PubMed  CAS  Google Scholar 

  • Ince P., Irving D., MacArthur F., and Perry R. H. (1991) Quantitative neuropathological study of Alzheimer-type pathology in the hippocampus: comparison of senile dementia of Alzheimer type, senile dementia of Lewy body type, Parkinson’s diseas and non-demented elderly control patients. J. Neurol. Sci. 106(2), 142–152.

    Article  PubMed  CAS  Google Scholar 

  • Ince P. G., McArthur F. K., Bjertness E., Torvik A., Candy J. M., and Edwardson J. A. (1995) Neuropathological diagnoses in elderly patients in Oslo: Alzheimer’s disease, Lewy body disease, vascular lesions. Dementia 6(3), 162–168.

    PubMed  CAS  Google Scholar 

  • Iwatsubo T., Yamaguchi H., Fujimuro M., et al. (1996) Purification and characterization of Lewy bodies from the brains of patients with diffuse Lewy body disease. Am. J. Pathol. 148(5), 1517–1529.

    PubMed  CAS  Google Scholar 

  • Jenco J. M., Rawlingson A., Daniels B., and Morris A. J. (1998) Regulation of phospholipase D2: selective inhibition of mammalian phospholipase D isoenzymes by alpha- and beta-synucleins. Biochemistry 37(14), 4901–4909.

    Article  PubMed  CAS  Google Scholar 

  • Kanda S., Bishop J. F., Eglitis M. A., Yang Y., and Mouradian M. M. (2000) Enhanced vulnerability to oxidative stress by alpha-synuclein mutations and C-terminal truncation. Neuroscience 97(2), 279–284.

    Article  PubMed  CAS  Google Scholar 

  • Kaufmann H., Hague K., and Perl D. (2001) Accumulation of alpha-synuclein in autonomic nerves in pure autonomic failure. Neurology 56(7), 980–981.

    PubMed  CAS  Google Scholar 

  • Ko L., Mehta N. D., Farrer M., Easson C., Hussey J., Yen S., Hardy J., and Yen S. H. (2000) Sensitization of neuronal cells to oxidative stress with mutated human alpha-synuclein. J. Neurochem. 75(6), 2546–2554.

    Article  PubMed  CAS  Google Scholar 

  • Kruger R., Kuhn W., Muller T., Woitalla D., Graeber M., Kosel S., et al. (1998) Ala30Pro mutation in the gene encoding alpha-synuclein in Parkinson’s disease [letter]. Nat. Genet. 18(2), 106–108.

    Article  PubMed  CAS  Google Scholar 

  • Lambert M. P., Barlow A. K., Chromy B. A., Edwards C., Freed R., Liosatos M., et al. (1998) Diffusible, nonfibrillar ligands derived from Abeta1–42 are potent central nervous system neurotoxins. Proc. Natl. Acad. Sci. USA 95(11), 6448–6453.

    Article  PubMed  CAS  Google Scholar 

  • Langston J. W., Ballard P., Tetrud J. W., and Irwin I. (1983) Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. Science 219(4587), 979–980.

    Article  PubMed  CAS  Google Scholar 

  • Lavedan C. (1998) The synuclein family. Genome Res. 8(9), 871–880.

    PubMed  CAS  Google Scholar 

  • Lee M., Hyun D., Halliwell B., and Jenner P. (2001) Effect of the overexpression of wild-type or mutant alpha-synuclein on cell susceptibility to insult. J. Neurochem. 76(4), 998–1009.

    Article  PubMed  CAS  Google Scholar 

  • Liberatore G. T., Jackson-Lewis V., Vukosavic S., Mandir A. S., Vila M., McAuliffe W. G., et al. (1999) Inducible nitric oxide synthase stimulates dopaminergic neurodegeneration in the MPTP model of Parkinson disease [see comments]. Nat. Med. 5(12), 1403–1409.

    Article  PubMed  CAS  Google Scholar 

  • Lindboe C. F. and Hansen H. B. (1998) The frequency of Lewy bodies in a consecutive autopsy series. Clin. Neuropathol. 17(4), 204–209.

    PubMed  CAS  Google Scholar 

  • Lippa C. F., Fujiwara H., Mann D. M., Giasson B., Baba M., Schmidt M. L., et al. (1998) Lewy bodies contain altered alpha-synuclein in brains of many familial Alzheimer’s disease patients with mutations in presenilin and amyloid precursor protein genes. Am. J. Pathol. 153(5), 1365–1370.

    PubMed  CAS  Google Scholar 

  • Lippa C. F., Schmidt M. L., Lee V. M., and Trojanowski J. Q. (1999) Antibodies to alpha-synuclein detect Lewy bodies in many Down’s syndrome brains with Alzheimer’s disease. Ann. Neurol. 45(3), 353–357.

    Article  PubMed  CAS  Google Scholar 

  • Lopez O. L., Wisniewski S., Hamilton R. L., Becker J. T., Kaufer D. I., and DeKosky S. T. (2000) Predictors of progression in patients with AD and Lewy bodies. Neurology 54(9), 1774–1779.

    PubMed  CAS  Google Scholar 

  • Lowe J., McDermott H., Landon M., et al. (1990) Ubiquitin carboxyl-terminal hydrolase (PGP9.5) is selectively present in ubiquitinated inclusion bodies characteristic of human neurodegenerative diseases. J. Pathol. 161(2), 153–160.

    Article  PubMed  CAS  Google Scholar 

  • Masliah E., Rockenstein E., Veinbergs I., Mallory M., Hashimoto M., Takeda A., et al. (2000) Dopaminergic loss and inclusion body formation in alpha-synuclein mice: implications for neurodegenerative disorders. Science 287(5456), 1265–1269.

    Article  PubMed  CAS  Google Scholar 

  • Mattson M. P., Barger S. W., Cheng B., Lieberburg I., Smith-Swintosky V. L., and Rydel R. E. (1993) beta-Amyloid precursor protein metabolites and loss of neuronal Ca2+ homeostasis in Alzheimer’s disease. Trends Neurosci. 16(10), 409–414.

    Article  PubMed  CAS  Google Scholar 

  • McGeer P. L. and McGeer E. G. (1995) The inflammatory response system of brain: implications for therapy of Alzheimer and other neurodegenerative diseases. Brain Res. Brain Res. Rev. 21(2), 195–218.

    Article  PubMed  CAS  Google Scholar 

  • McLean P. J., Kawamata H., Ribich S., and Hyman B. T. (2000) Membrane association and protein conformation of alpha-synuclein in intact neurons. Effect of Parkinson’s disease-linked mutations. J. Biol. Chem. 275(12), 8812–8816.

    Article  PubMed  CAS  Google Scholar 

  • Murphy D. D., Rueter S. M., Trojanowski J. Q., and Lee V. M. (2000) Synucleins are developmentally expressed, and alpha-synuclein regulates the size of the presynaptic vesicular pool in primary hippocampal neurons. J. Neurosci. 20(9), 3214–3220.

    PubMed  CAS  Google Scholar 

  • Narhi L., Wood S. J., Steavenson S., Jiang Y., Wu G. M., Anafi D., et al. (1999) Both familial Parkinson’s disease mutations accelerate alpha-synuclein aggregation. J. Biol. Chem. 274(14), 9843–9846.

    Article  PubMed  CAS  Google Scholar 

  • Newell K. L., Boyer P., Gomez-Tortosa E., Hobbs W., Hedley-Whyte E. T., Vonsattel J. P., and Hyman B. T. (1999) Alpha-synuclein immunoreactivity is present in axonal swellings in neuroaxonal dystrophy and acute traumatic brain injury. J. Neuropathol. Exp. Neurol. 58(12), 1263–1268.

    Article  PubMed  CAS  Google Scholar 

  • Ostrerova N., Petrucelli L., Farrer M., Mehta N., Choi P., Hardy J., and Wolozin B. (1999) alpha-Synuclein shares physical and functional homology with 14-3-3 proteins. J. Neurosci. 19(14), 5782–5791.

    PubMed  CAS  Google Scholar 

  • Ostrerova-Golts N., Petrucelli L., Hardy J., Lee J. M., Farer M., and Wolozin B. (2000) The A53T alpha-synuclein mutation increases iron-dependent aggregation and toxicity. J. Neurosci. 20(16), 6048–6054.

    PubMed  CAS  Google Scholar 

  • Parker W. D. Jr., Boyson S. J., and Parks J. K. (1989) Abnormalities of the electron transport chain in idiopathic Parkinson’s disease. Ann. Neurol. 26(6), 719–723.

    Article  PubMed  Google Scholar 

  • Polymeropoulos M. H., Lavedan C., Leroy E., Ide S. E., Dehejia A., Dutra A., et al. (1997) Mutation in the alpha-synuclein gene identified in families with Parkinson’s disease [see comments]. Science 276(5321), 2045–2047.

    Article  PubMed  CAS  Google Scholar 

  • Przedborski S. and Jackson-Lewis V. (1998) Mechanisms of MPTP toxicity. Mov. Disord. 13(Suppl 1), 35–38.

    PubMed  Google Scholar 

  • Rogers J., Webster S., Lue L. F., Brachova L., Civin W. H., Emmerling M., et al. (1996) Inflammation and Alzheimer’s disease pathogenesis. Neurobiol. Aging 17(5), 681–686.

    Article  PubMed  CAS  Google Scholar 

  • Saha A. R., Ninkina N. N., Hanger D. P., Anderton B. H., Davies A. M., and Buchman V. L. (2000) Induction of neuronal death by alpha-synuclein. Eur. J. Neurosci. 12(8), 3073–3077.

    Article  PubMed  CAS  Google Scholar 

  • Schapira A. H., Cooper J. M., Dexter D., Clark J. B., Jenner P., and Marsden C. D. (1990) Mitochondrial complex I deficiency in Parkinson’s disease. J. Neurochem. 54(3), 823–827.

    Article  PubMed  CAS  Google Scholar 

  • Schmidt M. L., Martin J. A., Lee V. M., and Trojanowski J. Q. (1996) Convergence of Lewy bodies and neurofibrillary tangles in amygdala neurons of Alzheimer’s disease and Lewy body disorders. Acta. Neuropathol. 91(5), 475–481.

    Article  PubMed  CAS  Google Scholar 

  • Schulz J. B., Matthews R. T., Klockgether T., Dichgans J., and Beal M. F. (1997) The role of mitochondrial dysfunction and neuronal nitric oxide in animal models of neurodegenerative diseases. Mol. Cell Biochem. 174(1–2), 193–197.

    Article  PubMed  CAS  Google Scholar 

  • Selkoe D. J. (2001) Alzhemier’s disease: genes, proteins, and therapy. Physiol. Rev. 81(2), 741–766.

    PubMed  CAS  Google Scholar 

  • Souza J. M., Giasson B. I., Chen Q., Lee V. M., and Ischiropoulos H. (2000) Dityrosine cross-linking promotes formation of stable alpha -synuclein polymers. Implication of nitrative and oxidative stress in the pathogenesis of neurodegenerative synucleinopathies. J. Biol. Chem. 275(24), 18,344–18,349.

    Article  CAS  Google Scholar 

  • Spillantini M. G., Crowther R. A., Jakes R., Cairns N. J., Lantos P. L., and Goedert M. (1998a) Filamentous alphasynuclein inclusions link multiple system atrophy with Parkinson’s disease and dementia with Lewy bodies. Neurosci. Lett. 251(3), 205–208.

    Article  PubMed  CAS  Google Scholar 

  • Spillantini M. G., Crowther R. A., Jakes R., Hasegawa M., and Goedert M. (1998b) alpha-Synuclein in filamentous inclusions of Lewy bodies from Parkinson’s disease and dementia with lewy bodies. Proc. Natl. Acad. Sci. USA 95(11), 6469–6473.

    Article  PubMed  CAS  Google Scholar 

  • Spillantini M. G., Schmidt M. L., Lee V. M., Trojanowski J. Q., Jakes R., and Goedert M. (1997) Alpha-synuclein in Lewy bodies [letter]. Nature 388(6645), 839–840.

    Article  PubMed  CAS  Google Scholar 

  • Swerdlow R. H., Parks J. K., Miller S. W., Tuttle J. B., Trimmer P. A., Sheehan J. P., et al. (1996) Origin and functional consequences of the complex I defect in Parkinson’s disease. Ann. Neurol. 40(4), 663–671.

    Article  PubMed  CAS  Google Scholar 

  • Tu P. H., Galvin J. E., Baba M., Giasson B., Tomita T., Leight S., et al. (1998) Glial cytoplasmic inclusions in white matter oligodendrocytes of multiple system atrophy brains contain insoluble alpha-synuclein. Ann. Neurol. 44(3), 415–422.

    Article  PubMed  CAS  Google Scholar 

  • Ueda K., Fukushima H., Masliah E., Xia Y., Iwai A., Yoshimoto M., et al. (1993) Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease. Proc. Natl. Acad. Sci. USA 90(23), 11,282–11,286.

    Article  CAS  Google Scholar 

  • Varadarajan S., Yatin S., Aksenova M., and Butterfield D. A. (2000) Review: Alzheimer’s amyloid beta-peptide-associated free radical oxidative stress and neurotoxicity. J. Struct. Biol. 130(2–3), 184–208.

    Article  PubMed  CAS  Google Scholar 

  • Wakabayashi K., Yoshimoto M., Fukushima T., Koide R., Horikawa Y., Morita T., and Takahashi H. (1999) Widespread occurrence of alpha-synuclein/NACP-immunoreactive neuronal inclusions in juvenile and adult-onset Hallervorden-Spatz disease with Lewy bodies. Neuropathol. Appl. Neurobiol. 25(5), 363–368.

    Article  PubMed  CAS  Google Scholar 

  • Weinreb P. H., Zhen W., Poon A. W., Conway K. A., and Lansbury P. T. Jr. (1996) NACP, a protein implicated in Alzheimer’s disease and learning, is natively unfolded. Biochemistry 35(43), 13,709–13,715.

    Article  CAS  Google Scholar 

  • Withers G. S., George J. M., Banker G. A., and Clayton D. F. (1997) Delayed localization of synelfin (synuclein, NACP) to presynaptic terminals in cultured rat hippocampal neurons. Brain Res. Dev. Brain Res. 99(1), 87–94.

    Article  PubMed  CAS  Google Scholar 

  • Zhou W., Hurlbert M. S., Schaack J., Prasad K. N., and Freed C. R. (2000) Overexpression of human alpha-synuclein causes dopamine neuron death in rat primary culture and immortalized mesencephalon-derived cells. Brain Res. 866(1–2), 33–43.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, PA

    Paul T. Kotzbauer, John Q. Trojanowski & Virginia M.-Y. Lee

Authors
  1. Paul T. Kotzbauer
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. John Q. Trojanowski
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Virginia M.-Y. Lee
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Virginia M.-Y. Lee.

Rights and permissions

Reprints and permissions

About this article

Cite this article

Kotzbauer, P.T., Trojanowski, J.Q. & Lee, V.MY. Lewy body pathology in Alzheimer’s disease. J Mol Neurosci 17, 225–232 (2001). https://doi.org/10.1385/JMN:17:2:225

Download citation

  • Received:

  • Accepted:

  • Issue Date:

  • DOI: https://doi.org/10.1385/JMN:17:2:225

Index Entries

Search

Navigation