Literature DB >> 2557056

Lewy bodies in Alzheimer disease--one or two diseases?

C Bergeron1, M Pollanen.   

Abstract

To clarify the significance of the Lewy body (LB) in Alzheimer disease (AD), we determined the incidence and distribution of LB in 150 cases of AD and 75 controls. We also examined the pathological changes in the substantia nigra and quantified neocortical alterations, including the density of neuritic plaques, neurofibrillary tangles, and LB. LBs were present in 25% of AD cases, but in only 5% of controls. The presence of LB was associated with significantly lower numbers of neurofibrillary tangles as compared with cases of AD without LB, whereas the mean density of neuritic plaques remained unchanged. Two possibilities are discussed to explain these findings. First, the high frequency of LB in AD may reflect a predisposition of AD patients to develop idiopathic Parkinson disease. Second, the LB may represent a nonspecific cytoskeletal change in selected vulnerable neuronal populations in some subjects with AD, rather than the presence of a second pathological process.

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Mesh:

Year:  1989        PMID: 2557056

Source DB:  PubMed          Journal:  Alzheimer Dis Assoc Disord        ISSN: 0893-0341            Impact factor:   2.703


  10 in total

1.  Characterization of a shared epitope in cortical Lewy body fibrils and Alzheimer paired helical filaments.

Authors:  M S Pollanen; C Bergeron; L Weyer
Journal:  Acta Neuropathol       Date:  1994       Impact factor: 17.088

2.  Diagnostic accuracy of Alzheimer's disease: a neuropathological study.

Authors:  O Kosunen; H Soininen; L Paljärvi; O Heinonen; S Talasniemi; P J Riekkinen
Journal:  Acta Neuropathol       Date:  1996       Impact factor: 17.088

3.  Twisted ribbon structure of paired helical filaments revealed by atomic force microscopy.

Authors:  M S Pollanen; P Markiewicz; C Bergeron; M C Goh
Journal:  Am J Pathol       Date:  1994-05       Impact factor: 4.307

4.  Altered neurofilament expression does not contribute to Lewy body formation.

Authors:  C Bergeron; C Petrunka; L Weyer; M S Pollanen
Journal:  Am J Pathol       Date:  1996-01       Impact factor: 4.307

5.  APOE4 exacerbates α-synuclein seeding activity and contributes to neurotoxicity in Alzheimer's disease with Lewy body pathology.

Authors:  Yunjung Jin; Fuyao Li; Berkiye Sonoustoun; Naveen Chandra Kondru; Yuka A Martens; Wenhui Qiao; Michael G Heckman; Tadafumi C Ikezu; Zonghua Li; Jeremy D Burgess; Danilyn Amerna; Justin O'Leary; Michael A DeTure; Jing Zhao; Pamela J McLean; Dennis W Dickson; Owen A Ross; Guojun Bu; Na Zhao
Journal:  Acta Neuropathol       Date:  2022-04-26       Impact factor: 15.887

6.  Absence of protease-resistant prion protein in dementia characterized by neuronal loss and status spongiosus.

Authors:  M S Pollanen; C Bergeron; L Weyer
Journal:  Acta Neuropathol       Date:  1993       Impact factor: 17.088

7.  Amyloid-Beta (Aβ) Plaques Promote Seeding and Spreading of Alpha-Synuclein and Tau in a Mouse Model of Lewy Body Disorders with Aβ Pathology.

Authors:  Fares Bassil; Hannah J Brown; Shankar Pattabhiraman; Joe E Iwasyk; Chantal M Maghames; Emily S Meymand; Timothy O Cox; Dawn M Riddle; Bin Zhang; John Q Trojanowski; Virginia M-Y Lee
Journal:  Neuron       Date:  2019-11-20       Impact factor: 17.173

8.  Evaluating the relationship between amyloid-β and α-synuclein phosphorylated at Ser129 in dementia with Lewy bodies and Parkinson's disease.

Authors:  Marta Swirski; J Scott Miners; Rohan de Silva; Tammaryn Lashley; Helen Ling; Janice Holton; Tamas Revesz; Seth Love
Journal:  Alzheimers Res Ther       Date:  2014-12-01       Impact factor: 6.982

Review 9.  α-synuclein in the pathophysiology of Alzheimer's disease.

Authors:  Daniel Twohig; Henrietta M Nielsen
Journal:  Mol Neurodegener       Date:  2019-06-11       Impact factor: 14.195

Review 10.  Interactions of amyloidogenic proteins.

Authors:  Benoit I Giasson; Virginia M-Y Lee; John Q Trojanowski
Journal:  Neuromolecular Med       Date:  2003       Impact factor: 4.103

  10 in total

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