Vascular degeneration in Parkinson's disease - PubMed (original) (raw)

Vascular degeneration in Parkinson's disease

Jian Guan et al. Brain Pathol. 2013 Mar.

Abstract

Vascular degeneration plays a significant role in contributing to neurodegenerative conditions such as Alzheimer's disease. Our understanding of the vascular components in Parkinson's disease (PD) is however limited. We have examined the vascular morphology of human brain tissue from both PD and the control cases using immunohistochemical staining and image analysis. The degenerative morphology seen in PD cases included the formation of endothelial cell "clusters," which may be contributed by the fragmentation of capillaries. When compared to the control cases, the capillaries of PDs were less in number (P < 0.001), shorter in length (P < 0.001) and larger in diameter (P < 0.01) with obvious damage to the capillary network evidenced by less branching (P < 0.001). The level of degeneration seen in the caudate nucleus was also seen in the age-matched control cases. Vessel degeneration associated with PD was, however, found in multiple brain regions, but particularly in the substantia nigra, middle frontal cortex and brain stem nuclei. The data suggest that vascular degeneration could be an additional contributing factor to the progression of PD. Thus, treatments that prevent vascular degeneration and improve vascular remodeling may be a novel target for the treatment of PD.

© 2012 The Authors; Brain Pathology © 2012 International Society of Neuropathology.

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Figures

Figure 1

Figure 1

Digital images of endothelial clusters (A,B, ×100), the capillaries from the

MFG

(C,D, ×10);

SN

(E,F, ×10);

RN

(G,H, ×20) in

PD

(right column) and control cases (left column). While the endothelial staining was evenly distributed in the capillaries of the control cases we found a large number of endothelial clusters (arrows) in the

PD

capillaries (A,B). Compared to the control cases, the number of capillaries in

PD

cases were less and shorter (C–F) and had larger diameters (G,H). Photos G,H are the inverted florescent images. Scale bars = 5 μm for A and B and 50 μm for C–H.

Figure 2

Figure 2

Graphs show changes in endothelial clusters. Compared to the age‐matched control cases (n = 6), the number of endothelial clusters (A) and the percentage of vessel area with clusters (B) were significantly increased in the

SN

,

CN

and

MFG

of the

PD

cases (n = 10, ***P < 0.001). Data presented as mean ±

SEM

.

Figure 3

Figure 3

Graphs show changes in vessel density. Compared to the age‐matched control cases (n = 6), the total vessel number was significantly less in the

SN

of

PD

cases (A, n = 10, *P < 0.01), but not in the

CN

and

MFG

. The number of vessels that were longer than 50 μm were significantly less in the

SN

and

MFG

of the

PD

cases compared to the control cases (B, ***P < 0.001). Data presented as mean ±

SEM

.

Figure 4

Figure 4

Graphs show changes in average length of blood vessels. Compared to the age‐matched control cases (n = 6), the average length of vessels were significantly shorter in the

MFG

of

PD

cases (A, n = 10, **P < 0.01) when the measurement included all vessels. The average length of the longer vessels (>50 μm) was significantly reduced in the

SN

and

MFG

of the

PD

cases compared to the control cases (B, **P < 0.01). Data presented as mean ±

SEM

.

Figure 5

Figure 5

Graph shows the number of branches of blood vessels. The number of branches was significantly less in the

SN

of the

PD

cases compared to the age‐matched control cases (*P < 0.05). Data presented as mean ±

SEM

.

Figure 6

Figure 6

Graphs show the changes in vessel size. Compared to the control cases (n = 4), the average diameter (A) and the average cross‐sectional area (B) of blood vessels were significantly increased in the

RN

of the

PD

cases (n = 6, *P < 0.05). Data presented as mean ±

SEM

.

Figure 7

Figure 7

Graphs show changes in vessel diameter. The number of vessels with diameters smaller than 10 μm was reduced in the

RN

and

LC

of the

PD

cases (A, n = 6, **P < 0.01), whereas the vessels with larger diameter (>10 μm) was increased in the

RN

of the

PD

cases (B, *P < 0.05). There was a significant reduction in the ratio of small/larger vessels in the

RN

and

LC

(C, *P < 0.05, **P < 0.01, C), but not in the

SN

.

References

    1. Abe Y, Yamamoto T, Soeda T, Kumagai T, Tanno Y, Kubo J et al (2009) Diabetic striatal disease: clinical presentation, neuroimaging, and pathology. Intern Med 48:1135–1141. -PubMed
    1. Arganda‐Carreras I, Fernández‐González R, Muñoz‐Barrutia A, Ortiz‐De‐Solorzano C (2010) 3D reconstruction of histological sections: application to mammary gland tissue. Microsc Res Tech 73:1019–1029. -PubMed
    1. Aston‐Jones G, Shipley MT, Chouvet G, van Ennis M, Bockstaele E, Pieribone V et al (1991) Afferent regulation of locus coeruleus neurons: anatomy, physiology and pharmacology. Prog Brain Res 88:47–75. -PubMed
    1. Bell RD, Winkler EA, Sagare AP, Singh I, LaRue B, Deane R, Zlokovic BV (2010) Pericytes control key neurovascular functions and neuronal phenotype in the adult brain and during brain aging. Neuron 68:409–427. -PMC -PubMed
    1. Bell RD, Winkler EA, Singh I, Sagare AP, Deane R, Wu Z et al (2012) Apolipoprotein E controls cerebrovascular integrity via cyclophilin A. Nature 485:512–516. -PMC -PubMed

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