A quantitative and ultrastructural study of substantia nigra and nucleus centralis superior in Alzheimer's disease

1985 ◽  
Vol 68 (3) ◽  
pp. 218-223 ◽  
Author(s):  
M. Tabaton ◽  
A. Schenone ◽  
P. Romagnoli ◽  
G. L. Mancardi
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Substantia Nigra ◽  
Ultrastructural Study

The 12th J. A. F. Stevenson Memorial Lecture: Aging, Alzheimer's disease, and the cholinergic system

1984 ◽  
Vol 62 (7) ◽  
pp. 741-754 ◽  
Author(s):  
Patrick L. McGeer
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Substantia Nigra ◽  
Locus Coeruleus ◽  
Basal Forebrain ◽  
Cholinergic System ◽  
Memory Storage ◽  
Substantia Nigra Pars Compacta ◽  
Memorial Lecture ◽  
Reticular Activating System

Aging does not affect tissues in a uniform fashion. Within the brain, substantial neuronal dropout occurs with age in the cholinergic medial basal forebrain complex, the noradrenergic locus coeruleus, and the dopaminergic substantia nigra pars compacta. These areas are also struck by diseases that are sharply age dependent. Alzheimer's disease causes neuronal destruction in the cholinergic cells of the medial basal forebrain and noradrenergic cells of the locus coeruleus. Parkinson's disease causes neuronal destruction mainly in the substantia nigra but with some destruction in the locus coeruleus. Parkinsonism–dementia affects all three areas. Alzheimer's disease is responsible for 50–60% of all cases of dementia. Severe dementia rises in frequency from less than 1% of the population at age 65–70 to over 15% by age 85. The cause of the disease is unknown. No method of prevention is known and present treatments are ineffective, although modest improvement has been reported for various therapeutic regimens designed to stimulate the cholinergic system. The neuronal systems identified as being affected in Alzheimer's disease and in the dementia of Parkinsonism correspond with those shown many years ago to be associated with the reticular activating system. This correspondence permits a new hypothesis of cognition and memory to be put forward, as well as a reinterpretation of data from animal research on the reticular activating system performed over a quarter of a century ago. The locus coeruleus is proposed as the noradrenergic element sensitizing the cortex to conscious recognition of real time events. The medial basal forebrain complex is proposed as the system registering the conscious event for storage and as the readout device when it is subsequently redisplayed in the cortex as memory. Storage could either be in the temporal lobe, in several areas of cortex with feedback to the medial basal forebrain, or in the cholinergic cells themselves.

The Lewy-Body Variant of Alzheimer's Disease

1993 ◽  
Vol 162 (3) ◽  
pp. 385-392 ◽  
Author(s):  
Hans Förstl ◽  
Alistair Burns ◽  
Phil Luthert ◽  
Nigel Cairns ◽  
Raymond Levy
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Substantia Nigra ◽  
Lewy Bodies ◽  
Cerebral Atrophy ◽  
Basal Nucleus ◽  
Course Of Illness ◽  
Alzheimer Type Dementia ◽  
Long Term Study ◽  
Duration Of Illness

At post-mortem, Lewy bodies (LBs) were found in the brainstem and neocortex of eight out of 65 patients who had been collected during a prospective long-term study on clinically diagnosed Alzheimer’s disease. All eight patients had accompanying Alzheimer pathology which was less severe than in a sample of eight age and sex-matched patients from the same study with neuropathologically verified Alzheimer's disease. Parkinsonian features were more common in patients with LBs. There were no particular differences in duration of illness, severity of cognitive impairment, presence of hallucinations, or fluctuations in the course of illness. Frontal cerebral atrophy was more marked in patients with LBs, as was the loss of neurons in the basal nucleus of Meynert and the substantia nigra. Cognitive performance correlated with the number of pigmented neurons in the substantia nigra. We conclude that the differential diagnosis of LB dementia should be considered in patients satisfying NINCDS-ADRDA criteria for Alzheimer-type dementia who show marked Parkinsonian features and a frontal accentuation of cerebral atrophy.

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