The Association of Ventral Tegmental Area Histopathology With Adult Dementia

Torack, Richard M.; Morris, John C.

doi:10.1001/archneur.1988.00520290025008

Cited by 169 publications

(54 citation statements)

References 26 publications

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“…The cholinergic neurons of the NBM and NDB and the amygdaloid nuclei, particularly the central, basal, and lateral nuclei, are provided with Table 1. dopaminergic innervation from the VTA and medial components of the SN (Sadikot and Parent 1990;Takada 1990;Gaykema and Zaborszky 1996;Zaborszky and Cullianan 1996). This may be important in some of the cognitive difficulties associated with damage to the mesolimbic DA system in Parkinson disease (Torack and Morris 1988), perhaps through modulation of the cholinergic system innervating the cortex (Zaborszky et al 1993). The amygdala has long been recognized as playing a role in emotional and affective experiences (Aggleton 1992).…”

Section: Discussionmentioning

confidence: 99%

Distribution of Dopamine D3 Receptor Expressing Neurons in the Human Forebrain Comparison with D2 Receptor Expressing Neurons

Gurevich

Joyce

1999

Neuropsychopharmacology

409

294

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Section: Discussionmentioning

confidence: 99%

Distribution of Dopamine D3 Receptor Expressing Neurons in the Human Forebrain Comparison with D2 Receptor Expressing Neurons

Gurevich

Joyce

1999

Neuropsychopharmacology

409

294

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“…Thus an altered PCC response to dopamine in patients with mood fluctuations may reflect abnormal dopaminergic modulation of caudate, anterior cingulate, or prefrontal cortex. One possible mechanism could be differential loss of dopamine innervation to these nuclei; no data directly address this possibility, but Torack and Morris (1988) did find greater cell loss in ventral tegmental area in PD patients with an antemortem diagnosis of depression.…”

Section: Posterior Cingulate Cortexmentioning

confidence: 91%

“…The relationship of dopamine to (nonfluctuating) depression in PD is unclear (Bunney et al, 1969;Jouvent et al, 1983;Mayeux et al, 1986;Torack and Morris, 1988;Cummings, 1992;Kostic et al, 1996;Black and Pandya, in press). By contrast, levodopa-related mood fluctuations in PD have a strongly face valid relationship to brain dopamine concentrations.…”

Section: Pharmacologymentioning

confidence: 99%

Levodopa Challenge Neuroimaging of Levodopa-Related Mood Fluctuations in Parkinson's Disease

Black

Hershey

Hartlein

et al. 2004

Neuropsychopharmacol

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Some patients with advanced Parkinson's disease (PD) develop dose-related fluctuations in mood. This may reflect alterations in dopamine-influenced brain circuits that mediate emotion. However, there is no available information to localize which dopamineinfluenced neurons may be most affected. Eight patients with PD and clinically significant levodopa-related mood fluctuations (mania, depression, or anxiety) were compared to 13 patients with similarly severe PD and fluctuations of motor function but not of mood. Regional cerebral blood flow (rCBF) was measured with positron emission tomography before and after levodopa (in the presence of carbidopa). The rCBF response to levodopa in medial frontal gyrus and posterior cingulate cortex (PCC) significantly differed between mood fluctuators and control patients (corrected po0.02). Other regions with uncorrected po0.001 in this comparison were cortical Brodmann areas 22, 40, 13, 11, and 28, hippocampus, and claustrum. The levodopa activation paradigm detected group differences not evident in a comparison of resting rCBF. Abnormalities of dopamine innervation may produce mood fluctuations via effects on PCC, an area strongly linked to mood and anxiety and with known rCBF responsiveness to levodopa or D2-like dopamine receptor agonists. We speculate that mood fluctuations may arise in parkinsonian patients who have abnormal dopaminergic modulation of caudate nucleus, anterior cingulate cortex, or orbital frontal cortex, all of which innervate PCC. The findings require confirmation in larger and bettermatched groups.

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“…There is also clear evidence that dopaminergic dysfunction also plays a role. Dopaminergic projections from the ventral tegmentum of the midbrain to the medial temporal and orbitofrontal regions are affected in post mortem studies (Torack & Morris, 1988).There is also evidence that limbic noradrenergic/dopaminergic pathways are dysfunctional in PD patients with depression compared to those without (Remy et al,2005). The main characteristics of depression are low mood and lack of interest or pleasure, one of which is required for a diagnosis of depression in most classifications.…”

Section: Depression and Anxietymentioning

confidence: 99%