scholarly journals Cerebral glucose metabolism and cognitive impairment in tremor-dominant and akinetic-rigid subtypes of Parkinson’s disease

2020 ◽  
Vol 12 (6) ◽  
pp. 42-48
Author(s):  
I. V. Miliukhina ◽  
Yu. G. Khomenko ◽  
E. V. Gracheva ◽  
G. V. Kataeva ◽  
E. A. Gromova

Parkinson’s disease (PD) is a disease characterized by marked phenotypic heterogeneity. The akinetic-rigid (AR) and tremor-dominant (TD) types of PD differ not only in motor manifestations, but also in the severity of non-motor symptoms, including cognitive impairment (CI). It is the PD heterogeneity study that can achieve the task of creating a modern personalized therapy for this disease.Objective: to study the characteristics of cerebral glucose metabolism in CI in patients with AR and TD PD.Patients and methods. Examinations were made in 69 patients with PD (the TD and AR subtypes were in 23 and 46 patients, respectively). Their cognitive status was assessed using the Mini-mental State Examination, the Montreal Cognitive Assessment, the Frontal Assessment Battery, and the Clock Drawing Test. 18F-fluorodeoxyglucose positron emission tomography was performed according to the standard procedure; glucose metabolism rate (GMR) was determined in different Brodmann areas (BA).Results and discussion. GMR in the frontal areas (right BA 6, 8, 9, 46 and left BA 46) was lower in the AR group that in the TD one (p< 0.05). The severity of CI in the AR group correlated with GMR in the parietal and posterior cingulate cortex (BA 7, 23, 26, 29, 30, and 31). The TD group showed correlations of the values of cognitive tests mainly with GMR in the frontal and anterior cingulate cortex (BA 6, 8–11, 24), and in the parietal (BA 7) and temporal cortices (BA 22). The only area, in which GMR correlated with cognitive performance in both groups, was BA 7.Conclusion. Two distinct patterns of GMR were identified in AR and TD within the general pattern of decreased cerebral glucose metabolism, which was specific for CI in PD. The findings may suggest that there are two different CI pathogenetic mechanisms associated with the clinical subtypes of PD.

2009 ◽  
Vol 24 (6) ◽  
pp. 854-862 ◽  
Author(s):  
Yoshiyuki Hosokai ◽  
Yoshiyuki Nishio ◽  
Kazumi Hirayama ◽  
Atsushi Takeda ◽  
Toshiyuki Ishioka ◽  
...  

2010 ◽  
Vol 64 (2) ◽  
pp. 65-73 ◽  
Author(s):  
Chul Hyoung Lyoo ◽  
Yong Jeong ◽  
Young Hoon Ryu ◽  
Juha O. Rinne ◽  
Myung Sik Lee

NeuroImage ◽  
1998 ◽  
Vol 7 (4) ◽  
pp. S237 ◽  
Author(s):  
M.L. Giroux ◽  
S.T. Grafton ◽  
J.R. Votaw ◽  
M.L. DeLong ◽  
J.M. Hoffman

2019 ◽  
Vol 20 (3) ◽  
pp. 696 ◽  
Author(s):  
Dong-Hee Choi ◽  
In-Ae Choi ◽  
Cheol Lee ◽  
Ji Yun ◽  
Jongmin Lee

The neuropathology of Parkinson’s disease with dementia (PDD) has been reported to involve heterogeneous and various disease mechanisms. Alpha-synuclein (α-syn) and amyloid beta (Aβ) pathology are associated with the cognitive status of PDD, and NADPH oxidase (NOX) is known to affect a variety of cognitive functions. We investigated the effects of NOX on cognitive impairment and on α-syn and Aβ expression and aggregation in PDD. In the 6-hydroxydopamine (6-OHDA)-injected mouse model, cognitive and motor function, and the levels of α-syn, Aβ, and oligomer A11 after inhibition of NOX4 expression in the hippocampal dentate gyrus (DG) were measured by the Morris water maze, novel object recognition, rotation, and rotarod tests, as well as immunoblotting and immunohistochemistry. After 6-OHDA administration, the death of nigrostriatal dopamine neurons and the expression of α-syn and NOX1 in the substantia nigra were increased, and phosphorylated α-syn, Aβ, oligomer A11, and NOX4 were upregulated in the hippocampus. 6-OHDA dose-dependent cognitive impairment was observed, and the increased cognitive impairment, Aβ expression, and oligomer A11 production in 6-OHDA-treated mice were suppressed by NOX4 knockdown in the hippocampal DG. Our results suggest that increased expression of NOX4 in the hippocampal DG in the 6-OHDA-treated mouse induces Aβ expression and oligomer A11 production, thereby reducing cognitive function.


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