Asset Details
Do you wish to reserve the book?
Morphometry of the human substantia nigra in ageing and Parkinson’s disease
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Morphometry of the human substantia nigra in ageing and Parkinson’s disease
Do you wish to request the book?
Morphometry of the human substantia nigra in ageing and Parkinson’s disease
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Morphometry of the human substantia nigra in ageing and Parkinson’s disease
2008
Overview
To investigate the relation between the loss of substantia nigra (SN) neurons in normal ageing and Parkinson’s disease (PD), we measured the total number and the cell body volume of pigmented (neuromelanin) neurons in the SN. We examined young (
n
= 7, mean age: 19.9), middle-aged (
n
= 9, mean age: 50.1), and older controls from the Baltimore Longitudinal Study of Aging (
n
= 7, mean age: 87.6), as well as PD cases (
n
= 8, mean age: 74.8). On random-systematically selected paraffin Nissl-stained sections, we used the Optical Fractionator to estimate the total number of neurons on one side of the SN. Using the Nucleator probe, we measured the volume of these neurons. In young and older controls, we also estimated the total number and volume of tyrosine hydroxylase (TH) positive (+) nigral neurons. We observed a significant loss of pigmented (-28.3%,
P
< 0.01) and TH (+) (−36.2%,
P
< 0.001) neurons in older controls compared with younger subjects. Analysis of the size distribution of pigmented and TH (+) neurons showed a significant hypertrophy in older controls compared to young controls (
P
< 0.01). In contrast, in PD we observed a significant atrophy of pigmented neurons compared to all control groups (
P
< 0.01). These data suggest that neuronal hypertrophy represents a compensatory mechanism within individual SN neurons that allows for normal motor function despite the loss of neurons in normal ageing. Presumably, this compensatory mechanism breaks down or is overwhelmed by the pathological events of PD leading to the onset of the characteristic motor disturbances.
