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Current Alzheimer Research

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

Different Morphology of Neuritic Plaques in the Archicortex of Alzheimer’s Disease with Comorbid Synucleinopathy: A Pilot Study

Author(s): Nikol Jankovska, Tomas Olejar*, Jaromir Kukal and Radoslav Matej

Volume 17, Issue 10, 2020

Page: [948 - 958] Pages: 11

DOI: 10.2174/1875692117999201215162043

Price: $65

Abstract

Background: Bulbous neuritic changes in neuritic plaques have already been described, and their possible effect on the clinical course of the disease has been discussed.

Objective: In our study, we focused on the location and density of these structures in patients with only Alzheimer’s disease (AD) and patients with AD in comorbidity with synucleinopathies.

Methods: Utilizing immunohistochemistry and confocal microscopy, we evaluated differences of neocortical and archicortical neuritic plaques and the frequency of bulbous changes in the archicortex of 14 subjects with Alzheimer’s disease (AD), 10 subjects with the Lewy body variant of Alzheimer's disease (AD/DLB), and 4 subjects with Alzheimer's disease with amygdala Lewy bodies (AD/ALB). Also, the progression and density of neuritic changes over the time course of the disease were evaluated.

Results: We found structural differences in bulbous dystrophic neurites more often in AD/DLB and AD/ALB than in pure AD cases. The bulbous neuritic changes were more prominent in the initial and progressive phases and were reduced in cases with a long clinical course.

Conclusion: Our results indicate that there is a prominent difference in the shape and composition of neocortical and archicortical neuritic plaques and, moreover, that bulbous neuritic changes can be observed at a higher rate in AD/DLB and AD/ALB subjects compared to pure AD subjects. This observation probably reflects that these subacute changes are more easily seen in the faster clinical course of AD patients with comorbidities.

Keywords: Alzheimer`s disease, synucleinopathy, archicortex, neocortex, neuritic plaques, bulbous neuritic changes.

« Previous
[1]
Nelson PT, Alafuzoff I, Bigio EH, et al. Correlation of Alzheimer disease neuropathologic changes with cognitive status: A review of the literature. J Neuropathol Exp Neurol 2012; 71(5): 362-81.
[http://dx.doi.org/10.1097/NEN.0b013e31825018f7] [PMID: 22487856]
[2]
Ellison D, Love S, Chimelli LMC, et al. Dementias in Neuropathology: A Reference Text of CNS Pathology. 3rd Edition Yong W. Elsevier Publishing 2012.
[3]
Knowles RB, Wyart C, Buldyrev SV, et al. Plaque-induced neurite abnormalities: implications for disruption of neural networks in Alzheimer’s disease. Proc Natl Acad Sci USA 1999; 96(9): 5274-9.
[http://dx.doi.org/10.1073/pnas.96.9.5274] [PMID: 10220456]
[4]
Malek-Ahmadi M, Perez SE, Chen K, Mufson EJ. Neuritic and diffuse plaque associations with memory in non-cognitively impaired elderly. J Alzheimers Dis 2016; 53(4): 1641-52.
[http://dx.doi.org/10.3233/JAD-160365] [PMID: 27540968]
[5]
Nelson PT, Braak H, Markesbery WR. Neuropathology and cognitive impairment in Alzheimer disease: a complex but coherent relationship. J Neuropathol Exp Neurol 2009; 68(1): 1-14.
[http://dx.doi.org/10.1097/NEN.0b013e3181919a48] [PMID: 19104448]
[6]
Qiu W-Y, Yang Q, Zhang W, et al. The correlations between postmortem brain pathologies and cognitive dysfunction in aging and Alzheimer’s disease. Curr Alzheimer Res 2018; 15(5): 462-73.
[http://dx.doi.org/10.2174/1567205014666171106150915] [PMID: 29110614]
[7]
Xiong F, Ge W, Ma C. Quantitative proteomics reveals distinct composition of amyloid plaques in Alzheimer’s disease. Alzheimers Dement 2019; 15(3): 429-40.
[http://dx.doi.org/10.1016/j.jalz.2018.10.006] [PMID: 30502339]
[8]
Xu B, Gao Y, Zhan S, et al. Quantitative protein profiling of hippocampus during human aging. Neurobiol Aging 2016; 39: 46-56.
[http://dx.doi.org/10.1016/j.neurobiolaging.2015.11.029] [PMID: 26923401]
[9]
Furcila D, DeFelipe J, Alonso-Nanclares L. A study of amyloid-β and phosphotau in plaques and neurons in the hippocampus of Alzheimer’s disease patients. J Alzheimers Dis 2018; 64(2): 417-35.
[http://dx.doi.org/10.3233/JAD-180173] [PMID: 29914033]
[10]
Montine TJ, Phelps CH, Beach TG, et al. National Institute on Aging; Alzheimer’s Association. National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease: a practical approach. Acta Neuropathol 2012; 123(1): 1-11.
[http://dx.doi.org/10.1007/s00401-011-0910-3] [PMID: 22101365]
[11]
Thal DR, Härtig W, Schober R. Stage-correlated distribution of type 1 and 2 dystrophic neurites in cortical and hippocampal plaques in Alzheimer’s disease. J Hirnforsch 1998; 39(2): 175-81.
[PMID: 10022341]
[12]
Davis DG, Wang HZ, Markesbery WR. Neocortical neuropil threads in Alzheimer’s, Pick’s, and diffuse Lewy body disease and in progressive supranuclear palsy. J Neuropathol Exp Neurol 1992; 51: 324.
[http://dx.doi.org/10.1097/00005072-199211000-00004]
[13]
Dickson DW, Crystal H, Mattiace LA, et al. Diffuse Lewy body disease: light and electron microscopic immunocytochemistry of senile plaques. Acta Neuropathol 1989; 78(6): 572-84.
[http://dx.doi.org/10.1007/BF00691284] [PMID: 2683563]
[14]
Outeiro TF, Koss DJ, Erskine D, et al. Dementia with Lewy bodies: an update and outlook. Mol Neurodegener 2019; 14(1): 5.
[http://dx.doi.org/10.1186/s13024-019-0306-8] [PMID: 30665447]
[15]
Hansen L, Salmon D, Galasko D, et al. The Lewy body variant of Alzheimer’s disease: a clinical and pathologic entity. Neurology 1990; 40(1): 1-8.
[http://dx.doi.org/10.1212/WNL.40.1.1] [PMID: 2153271]
[16]
Hansen LA. The Lewy body variant of Alzheimer disease. J Neural Transm Suppl 1997; 51: 83-93.
[http://dx.doi.org/10.1007/978-3-7091-6846-2_7] [PMID: 9470130]
[17]
Pollanen MS, Dickson DW, Bergeron C. Pathology and biology of the Lewy body. J Neuropathol Exp Neurol 1993; 52(3): 183-91.
[http://dx.doi.org/10.1097/00005072-199305000-00001] [PMID: 7684074]
[18]
Lippa CF, Smith TW, Swearer JM. Alzheimer’s disease and Lewy body disease: a comparative clinicopathological study. Ann Neurol 1994; 35(1): 81-8.
[http://dx.doi.org/10.1002/ana.410350113] [PMID: 8285597]
[19]
Armstrong TP, Hansen LA, Salmon DP, et al. Rapidly progressive dementia in a patient with the Lewy body variant of Alzheimer’s disease. Neurology 1991; 41(8): 1178-80.
[http://dx.doi.org/10.1212/WNL.41.8.1178] [PMID: 1714056]
[20]
Uchikado H, Lin W-L, DeLucia MW, Dickson DW. Alzheimer disease with amygdala Lewy bodies: a distinct form of α-synucleinopathy. J Neuropathol Exp Neurol 2006; 65(7): 685-97.
[http://dx.doi.org/10.1097/01.jnen.0000225908.90052.07] [PMID: 16825955]
[21]
Van Dam D, Vermeiren Y, Dekker AD, Naudé PJW, Deyn PP. Neuropsychiatric disturbances in Alzheimer’s disease: what have we learned from neuropathological studies? Curr Alzheimer Res 2016; 13(10): 1145-64.
[http://dx.doi.org/10.2174/1567205013666160502123607] [PMID: 27137218]
[22]
Lopez OL, Wisniewski S, Hamilton RL, Becker JT, Kaufer DI, DeKosky ST. Predictors of progression in patients with AD and Lewy bodies. Neurology 2000; 54(9): 1774-9.
[http://dx.doi.org/10.1212/WNL.54.9.1774] [PMID: 10802783]
[23]
Olichney JM, Galasko D, Salmon DP, et al. Cognitive decline is faster in Lewy body variant than in Alzheimer’s disease. Neurology 1998; 51(2): 351-7.
[http://dx.doi.org/10.1212/WNL.51.2.351] [PMID: 9710002]
[24]
Del-Ser T, Munoz DG, Hachinski V. Temporal pattern of cognitive decline and incontinence is different in Alzheimer’s disease and diffuse Lewy body disease. Neurology 1996; 46(3): 682-6.
[http://dx.doi.org/10.1212/WNL.46.3.682] [PMID: 8618667]
[25]
Gao Y, Tan L, Yu J-T, Tan L. Tau in Alzheimer’s disease: mechanisms and therapeutic strategies. Curr Alzheimer Res 2018; 15(3): 283-300.
[http://dx.doi.org/10.2174/1567205014666170417111859] [PMID: 28413986]
[26]
Hyman BT, Phelps CH, Beach TG, et al. National Institute on Aging-Alzheimer’s Association guidelines for the neuropathologic assessment of Alzheimer’s disease. Alzheimers Dement 2012; 8(1): 1-13.
[http://dx.doi.org/10.1016/j.jalz.2011.10.007] [PMID: 22265587]
[27]
Braak H, Alafuzoff I, Arzberger T, Kretzschmar H, Del Tredici K. Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry. Acta Neuropathol 2006; 112(4): 389-404.
[http://dx.doi.org/10.1007/s00401-006-0127-z] [PMID: 16906426]
[28]
McKeith IG, Boeve BF, Dickson DW, et al. Diagnosis and management of dementia with Lewy bodies: Fourth consensus report of the DLB Consortium. Neurology 2017; 89(1): 88-100.
[http://dx.doi.org/10.1212/WNL.0000000000004058] [PMID: 28592453]
[29]
Duyckaerts C, Dickson DW. Neurodegeneration: the molecular pathology of dementia and movement disorders. Wiley-Blackwell Publishing 2011; pp. 68-71.
[30]
Vickers JC, Mitew S, Woodhouse A, et al. Defining the earliest pathological changes of Alzheimer’s disease. Curr Alzheimer Res 2016; 13(3): 281-7.
[http://dx.doi.org/10.2174/1567205013666151218150322] [PMID: 26679855]
[31]
D’Amore JD, Kajdasz ST, McLellan ME, Bacskai BJ, Stern EA, Hyman BT. In vivo multiphoton imaging of a transgenic mouse model of Alzheimer disease reveals marked thioflavine-S-associated alterations in neurite trajectories. J Neuropathol Exp Neurol 2003; 62(2): 137-45.
[http://dx.doi.org/10.1093/jnen/62.2.137] [PMID: 12578223]
[32]
He Z, Guo JL, McBride JD, et al. Amyloid-β plaques enhance Alzheimer’s brain tau-seeded pathologies by facilitating neuritic plaque tau aggregation. Nat Med 2018; 24(1): 29-38.
[http://dx.doi.org/10.1038/nm.4443] [PMID: 29200205]
[33]
Dickson DW, Ruan D, Crystal H, et al. Hippocampal degeneration differentiates diffuse Lewy body disease (DLBD) from Alzheimer’s disease: light and electron microscopic immunocytochemistry of CA2-3 neurites specific to DLBD. Neurology 1991; 41(9): 1402-9.
[http://dx.doi.org/10.1212/WNL.41.9.1402] [PMID: 1653914]
[34]
Harrington CR, Perry RH, Perry EK, et al. Senile dementia of Lewy body type and Alzheimer type are biochemically distinct in terms of paired helical filaments and hyperphosphorylated tau protein. Dementia 1994; 5(5): 215-28.
[PMID: 7951676]
[35]
Strong C, Anderton BH, Perry RH, Perry EK, Ince PG, Lovestone S. Abnormally phosphorylated tau protein in senile dementia of Lewy body type and Alzheimer disease: evidence that the disorders are distinct. Alzheimer Dis Assoc Disord 1995; 9(4): 218-22.
[http://dx.doi.org/10.1097/00002093-199509040-00008] [PMID: 8749611]
[36]
Ince P, Irving D, MacArthur F, Perry RH. Quantitative neuropathology in the hippocampus: comparison of senile dementia of Alzheimer type, senile dementia of Lewy body type, Parkinson’s disease and non-demented elderly control patients. J Neurol Sci 1991; 106: 142-52.
[http://dx.doi.org/10.1016/0022-510X(91)90251-2] [PMID: 1802962]
[37]
Gurel B, Cansev M, Koc C, et al. Proteomics analysis of CA1 region of the hippocampus in pre-, progression and pathological stages in a mouse model of the Alzheimer’s disease. Curr Alzheimer Res 2019; 16(7): 613-21.
[http://dx.doi.org/10.2174/1567205016666190730155926] [PMID: 31362689]
[38]
Wee M, Chegini F, Power JHT, Majd S. Tau positive neurons show marked Mitochondrial loss and nuclear degradation in Alzheimer’s disease. Curr Alzheimer Res 2018; 15(10): 928-37.
[http://dx.doi.org/10.2174/1567205015666180613115644] [PMID: 29895248]
[39]
Connor DJ, Salmon DP, Sandy TJ, Galasko D, Hansen LA, Thal LJ. Cognitive profiles of autopsy-confirmed Lewy body variant vs pure Alzheimer disease. Arch Neurol 1998; 55(7): 994-1000.
[http://dx.doi.org/10.1001/archneur.55.7.994] [PMID: 9678318]
[40]
Terry RD, Masliah E, Hansen LA. Structural basis of the cognitive alterations in Alzheimer disease. Iven Press 1994; pp. 179-96.
[41]
Wisniewski HM, Vorbrodt AW, Moretz RC, Lossinsky AS, Grundke-Iqbal I. Pathogenesis of neuritic (senile) and amyloid plaque formation. Exp Brain Res 1982; (5): 3-9.
[PMID: 6891336]
[42]
Serrano-Pozo A, Betensky RA, Frosch MP, Hyman BT. plaque-associated local toxicity increases over the clinical course of Alzheimer disease. Am J Pathol 2016; 186(2): 375-84.
[http://dx.doi.org/10.1016/j.ajpath.2015.10.010] [PMID: 26687817]

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