Amygdala pathology in Parkinson's disease

Braak, Heiko; Yilmazer, D.; Vos, Rob A. I. de; Jansen, E. N. H.; Bohl, J.; Jellinger, K. A.

doi:10.1007/s004010050191

Cited by 112 publications

(141 citation statements)

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“…There is also considerable evidence for dysfunction of the mesolimbic dopaminergic system in PD, since the orbitofrontal and amygdalar presynaptic dopaminergic functions are also altered in early PD (Bazzett and Becker 1994;Ouchi et al 1999). In the present study, our results showed that DA release from the CAN of PD rats was seriously affected, similar to the results of other studies which showed morphological changes in the amygdala of PD patients (Braak et al 1994;Braak and Braak 2000). Interestingly, the impaired DA release from the lesioned left side was restored to a level similar to that in non-PD control rats by EB treatment (Fig.…”

Section: Discussionsupporting

confidence: 90%

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Increased dopamine release in vivo by estradiol benzoate from the central amygdaloid nucleus of Parkinson's disease model rats

Liu

Xie

2004

Journal of Neurochemistry

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In addition to the dopaminergic neurons in the nigrostriatal system, the properties of dopaminergic neurons in the mesolimbic system, such as the amygdala, are also of interest and importance because of their specific neuromodulatory effects in the pathophysiology of Parkinson's disease (PD). Using the fast cyclic voltammetry (FCV) technique, we present evidence to indicate that electrically-evoked dopamine (DA) release from the amygdala, especially the central amygdaloid nucleus (CAN), of ovariectomized (OVX) female rats was significantly enhanced with increasing doses of estradiol benzoate (EB; 30, 50 and 100 lg/kg). Impaired DA release from the amygdala of an OVX rat PD model can also be increased by EB treatment (50 lg/kg) to a level similar to that of controls. The well established neuroprotective effects of estrogen may be beneficial for reducing the dysfunction of dopaminergic neurons in mesolimbic structures of rat PD models and PD patients.

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Section: Discussionsupporting

confidence: 90%

“…Post-mortem studies have revealed severe neuropathological changes, characterized by the presence of Lewy bodies, in both the accessory cortical nucleus and the central nucleus of the amygdala in PD (Braak et al 1994). Such pathologies may underlie the emotional deficits which accompany PD (Tessitore et al 2002).…”

mentioning

confidence: 99%

Increased dopamine release in vivo by estradiol benzoate from the central amygdaloid nucleus of Parkinson's disease model rats

Liu

Xie

2004

Journal of Neurochemistry

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“…Research in the last 25 years has confirmed that although the lesion in the SN is a key hallmark to the pathological confirmation of PD, the pathological lesions are much more extensive and involve a number of pathways in the brainstem and areas of the neocortex [18,56,57]. It is presentlyrecognizedthat early neuronal loss occurs in other regions involved in motor control [58,59] and in neurons of the mesocortical system [60].…”

Section: Pathology Spreading and Neuronal Circuits Affectedmentioning

confidence: 99%

Revisiting oxidative stress and mitochondrial dysfunction in the pathogenesis of Parkinson disease—resemblance to the effect of amphetamine drugs of abuse

Perfeito

Cunha‐Oliveira

Rego

2012

Free Radical Biology and Medicine

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“…PD shows a different selective neuronal vulnerability than AD [135,154] and it is unknown to which extend the cell-type-specific pattern of Levy body formation and neurodegeneration in PD matches the pattern of neurons that show accumulation of nDNA damage but no cell loss during aging. However, the most prominent cell loss in PD affects the dopaminergic neurons in the substantia nigra pars compacta (SN pc ) [154,155].…”

Section: Accumulation Of Ndna Damage or Neuron Loss: Implications Formentioning

confidence: 99%

Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

et al. 2008

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According to a long-standing hypothesis, aging is mainly caused by accumulation of nuclear (n) DNA damage in differentiated cells such as neurons due to insufficient nDNA repair during lifetime. In line with this hypothesis it was until recently widely accepted that neuron loss is a general consequence of normal aging, explaining some degree of decline in brain function during aging. However, with the advent of more accurate procedures for counting neurons, it is currently widely accepted that there is widespread preservation of neuron numbers in the aging brain, and the changes that do occur are relatively specific to certain brain regions and types of neurons. Whether accumulation of nDNA damage and decline in nDNA repair is a general phenomenon in the aging brain or also shows cell-type specificity is, however, not known. It has not been possible to address this issue with the biochemical and molecular-biological methods available to study nDNA damage and nDNA repair. Rather, it was the introduction of autoradiographic methods to study quantitatively the relative amounts of nDNA damage (measured as nDNA single-strand breaks) and nDNA repair (measured as unscheduled DNA synthesis) on tissue sections that made it possible to address this question in a cell-type-specific manner under physiological conditions. The results of these studies revealed a formerly unknown inverse relationship between age-related accumulation of nDNA damage and age-related impairment in nDNA repair on the one hand, and the age-related, selective, loss of neurons on the other hand. This inverse relation may not only reflect a fundamental process of aging in the central nervous system but also provide the molecular basis for a new approach to understand the selective neuronal vulnerability in neurodegenerative diseases, particularly Alzheimer's disease.

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Amygdala pathology in Parkinson's disease

Cited by 112 publications

References 0 publications

Increased dopamine release in vivo by estradiol benzoate from the central amygdaloid nucleus of Parkinson's disease model rats

Increased dopamine release in vivo by estradiol benzoate from the central amygdaloid nucleus of Parkinson's disease model rats

Revisiting oxidative stress and mitochondrial dysfunction in the pathogenesis of Parkinson disease—resemblance to the effect of amphetamine drugs of abuse

Accumulation of nuclear DNA damage or neuron loss: Molecular basis for a new approach to understanding selective neuronal vulnerability in neurodegenerative diseases

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