Parkinson's disease: Neuron loss in the nucleus basalis without concomitant Alzheimer's disease
β Scribed by Imaharu Nakano; Dr Asao Hirano
- Publisher
- John Wiley and Sons
- Year
- 1984
- Tongue
- English
- Weight
- 787 KB
- Volume
- 15
- Category
- Article
- ISSN
- 0364-5134
No coin nor oath required. For personal study only.
β¦ Synopsis
A representative region of the nucleus basalis of Meynert was investigated in 11 patients with idiopathic Parkinson's disease and compared with the identical region in 13 age-matched control subjects. Simultaneously, the cerebral cortex and the nucleus basalis i n the patients with Parkinson's disease were examined for senile plaques and Alzheimer's neurofibrillary tangles. The nucleus basalis was significantly depleted of its large neurons in Parkinson's disease (p < 0.001 versus controls; Student t test), but in the majority of cases the neuron loss was not associated with Alzheimer's disease.
π SIMILAR VOLUMES
This research was carried out during the tenure of a postdoctoral fellowship from the Muscular Dystrophy Association awarded to Dr Argov. We thank Dr N. R. M. Buist for his ongoing interest in this case and the support of his Muscular Dystrophy Association grant.
Recent studies indicate that there is a marked reduction in trkA-containing nucleus basalis neurons in end-stage Alzheimer's disease (AD). We used unbiased stereological counting procedures to determine whether these changes extend to individuals with mild cognitive impairment (MCI) without dementia
## Abstract Precise placement of the electrodes for stimulation of the subthalamic nucleus (STN) in Parkinson's disease (PD) is crucial for the therapeutic benefit. As a result of the mistargeting and misplacement of the electrodes during surgery in 2 patients with PD, we have characterized the neu
## Abstract A depletion of large cholinergic neurons in the nucleus basalis of Meynert is a consistent finding in Alzheimer's disease (AD). The nucleus basalis of Meynert also contains interneurons and afferents that may modulate its functioning. In the present study we examined neurochemical marke