Abstract
Neurochemical research in dementia needs to move beyond descriptive inventories of neurotransmitter systems affected in the specific disorders and to link to molecular studies of mechanism and clinical studies of cognition. New advances in Alzheimer's Disease (AD), Huntington's Disease (HD), and Parkinson's Disease (PD) are being guided by models of how nerve cells die in these disorders. Theories of pathophysiology which address the cellular level need to explain the selective vulnerability of neuronal populations in the different diseases. Clinically, the importance of neurochemical studies will be increased by understanding the bridges between neural and cognitive processes. Clinicians are concerned about the nosology of dementias, diagnostic tests, and more effective therapies. The value of neurochemical studies will be enhanced to the extent that they can contribute to understanding and modifying the clinical phenomenology of these disorders. In this paper, we will briefly review what is known about the neurochemistry of dementia but focus most of our attention on establishing the linkage between this level of description and the levels of description which are either "downstream" (molecular biology) or "upstream" (cognition) in terms of a reductionistic conception of understanding the disease process. We will explore how understanding neurochemistry relates to our understanding of disease mechanism and what constraints neurochemical studies place on understanding clinical aspects of disease. We will conclude by briefly discussing some of the problems with our current understanding of the neurochemistry of dementia and how we can address those problems in the future.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 131-142 |
| Number of pages | 12 |
| Journal | Progress in Clinical and Biological Research |
| Volume | 317 |
| State | Published - 1989 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Medicine(all)
Cite this
Neurochemistry of dementia : establishing the links. / Whitehouse, P. J.; Gambetti, P.; Harik, S. I.; Kalaria, R. N.; Perry, G.; Younkin, Steven G; Tabaton, M.; Unnerstall, J. R.
In: Progress in Clinical and Biological Research, Vol. 317, 1989, p. 131-142.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Neurochemistry of dementia
T2 - establishing the links.
AU - Whitehouse, P. J.
AU - Gambetti, P.
AU - Harik, S. I.
AU - Kalaria, R. N.
AU - Perry, G.
AU - Younkin, Steven G
AU - Tabaton, M.
AU - Unnerstall, J. R.
PY - 1989
Y1 - 1989
N2 - Neurochemical research in dementia needs to move beyond descriptive inventories of neurotransmitter systems affected in the specific disorders and to link to molecular studies of mechanism and clinical studies of cognition. New advances in Alzheimer's Disease (AD), Huntington's Disease (HD), and Parkinson's Disease (PD) are being guided by models of how nerve cells die in these disorders. Theories of pathophysiology which address the cellular level need to explain the selective vulnerability of neuronal populations in the different diseases. Clinically, the importance of neurochemical studies will be increased by understanding the bridges between neural and cognitive processes. Clinicians are concerned about the nosology of dementias, diagnostic tests, and more effective therapies. The value of neurochemical studies will be enhanced to the extent that they can contribute to understanding and modifying the clinical phenomenology of these disorders. In this paper, we will briefly review what is known about the neurochemistry of dementia but focus most of our attention on establishing the linkage between this level of description and the levels of description which are either "downstream" (molecular biology) or "upstream" (cognition) in terms of a reductionistic conception of understanding the disease process. We will explore how understanding neurochemistry relates to our understanding of disease mechanism and what constraints neurochemical studies place on understanding clinical aspects of disease. We will conclude by briefly discussing some of the problems with our current understanding of the neurochemistry of dementia and how we can address those problems in the future.
AB - Neurochemical research in dementia needs to move beyond descriptive inventories of neurotransmitter systems affected in the specific disorders and to link to molecular studies of mechanism and clinical studies of cognition. New advances in Alzheimer's Disease (AD), Huntington's Disease (HD), and Parkinson's Disease (PD) are being guided by models of how nerve cells die in these disorders. Theories of pathophysiology which address the cellular level need to explain the selective vulnerability of neuronal populations in the different diseases. Clinically, the importance of neurochemical studies will be increased by understanding the bridges between neural and cognitive processes. Clinicians are concerned about the nosology of dementias, diagnostic tests, and more effective therapies. The value of neurochemical studies will be enhanced to the extent that they can contribute to understanding and modifying the clinical phenomenology of these disorders. In this paper, we will briefly review what is known about the neurochemistry of dementia but focus most of our attention on establishing the linkage between this level of description and the levels of description which are either "downstream" (molecular biology) or "upstream" (cognition) in terms of a reductionistic conception of understanding the disease process. We will explore how understanding neurochemistry relates to our understanding of disease mechanism and what constraints neurochemical studies place on understanding clinical aspects of disease. We will conclude by briefly discussing some of the problems with our current understanding of the neurochemistry of dementia and how we can address those problems in the future.
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M3 - Article
C2 - 2574868
AN - SCOPUS:0024795709
VL - 317
SP - 131
EP - 142
JO - Progress in Clinical and Biological Research
JF - Progress in Clinical and Biological Research
SN - 0361-7742
ER -