Dendritic changes in the basal nucleus of meynert and in the diagonal band nucleus in Alzheimer's disease—A quantitative Golgi investigation

Neuroscience ◽  
1986 ◽  
Vol 19 (4) ◽  
pp. 1265-1278 ◽  
Author(s):  
T. Arendt ◽  
H.G. Zveuintshva ◽  
T.A. Lkontovich
1992 ◽  
Vol 22 (4) ◽  
pp. 877-884 ◽  
Author(s):  
Hans Förstl ◽  
Alistair Burns ◽  
Philip Luthert ◽  
Nigel Cairns ◽  
Peter Lantos ◽  
...  

SynopsisDepressive symptoms have been reported in patients with mild to moderate Alzheimer's disease (AD). Recent evidence suggests that a noradrenergic deficit originating from neuronal degeneration in brainstem nuclei may represent an organic correlate of these disturbances. We examined the neuropathological changes in the locus coeruleus (LC), substantia nigra (SN), basal nucleus of Meynert and cortex of 52 patients (12 male, 40 female, mean age 83·2 ± 6·4 years) with pathologically verified AD. Fourteen patients (1 male, 13 female) showed signs of depression. The majority of these patients suffered from severe physical disability or sensory impairment and developed persistent delusions, but had less cognitive impairment. Neuronal counts in the LC were significantly lower than in the 38 patients without depression (36·9 ± 14 ·0; 51·4 ± 28·0 neuromelaninpigmented cells per section per nucleus;F= 3·4, df = 1, 50,P= 0·04). Neuron counts were higher in the basal nucleus of Meynert in depressed AD patients and there were no differences of the neuron numbers in the SN. Depression (main effect;F= 4·5,P= 0·04) contributed significantly to the variance of neuronal counts in the LC, even when covarying for gender, age of onset, cognitive impairment and cortical Alzheimer pathology. The observed disproportionate loss of noradrenergic and cholinergic neurons in the LC and basal nucleus of Meynert may represent an important organic substrate of depression in AD.


2000 ◽  
Vol 100 (3) ◽  
pp. 259-269 ◽  
Author(s):  
I. Sassin ◽  
C. Schultz ◽  
D. R. Thal ◽  
U. Rüb ◽  
K. Arai ◽  
...  

1989 ◽  
Vol 504 (2) ◽  
pp. 354-357 ◽  
Author(s):  
Kiyomitsu Oyanagi ◽  
Hitoshi Takahashi ◽  
Koichi Wakabayashi ◽  
Fusahiro Ikuta

1989 ◽  
Vol 78 (1) ◽  
pp. 90-95 ◽  
Author(s):  
O. J. M. Vogels ◽  
K. Renkawek ◽  
C. A. J. Broere ◽  
H. J. ter Laak ◽  
F. van Workum

2020 ◽  
Vol 9 (1) ◽  
pp. 77-85
Author(s):  
T. A. Ishunina ◽  
I. N. Bogolepova ◽  
D. F. Swaab

The article focuses on age-related morphofunctional changes in the human brain and the issue of compensatory-adaptive mechanisms developed in normal aging. According to the scientific literature, the volume of white matter is reduced to a greater extent with aging, the fact associating with myelin fibers degeneration, the appearance of Virchow–Robin spaces and a decrease in the effectiveness of the blood-brain barrier. Atrophic processes in gray matter are currently associated not only with the death of neurons, but with degenerative changes in synapses, a decrease in their number, and reduction of dendritic branches and spines. A decrease in the size of pericarions resulting in a decrease in the number of large neurocytes and an increase in the proportion of small neurons is noted in certain brain structures. However, age-related neuronal hypertrophy is observed in the nuclei of the hypothalamus, Meinert’s basal nucleus. This is mostly manifested in the female group, and is undoubtedly associated with a decrease in estrogen levels and the period of menopause. An increase in the metabolic activity of neurons manifested by related changes in the size of the pericarions and nuclei of neurons and their Golgi complex can be attributed to compensatory-adaptive mechanisms that can delay or prevent the development of neurodegenerative disorders, such as Alzheimer's disease. Neurons with a higher metabolic activity have better ability to self-repair. Due to this, neuron reactivation techniques are being developed with aging based on the selection of the correct stimulus. The growth of the glial cell population is also considered to be compensatory, since these cells are crucial for neuron adaptation and able to affect the level of neuronal RNA synthesis. Furthermore, the article highlights literature data on possible triggers of the compensatory capabilities of the brain with aging and under pathological processes.


1993 ◽  
Vol 163 (3) ◽  
pp. 364-368 ◽  
Author(s):  
Hans Förstl ◽  
Alistair Burns ◽  
Raymond Levy ◽  
Nigel Cairns ◽  
Philip Luthert ◽  
...  

Clinico-pathological correlations were examined in 54 patients with neuropathologically verified Alzheimer's disease (AD) who were part of a prospective study. Behavioural disturbance was documented using an expanded version of the Stockton Geriatric Rating Scale (SGRS). The subscores for physical disability (P), apathy (A) and communication failure (C) (summation score PAC) were closely correlated and were high in most patients during the late stages of illness. High PAC scores correlated with an earlier onset and longer duration of illness, lower brain weight, more severe tangle pathology in the parahippocampal gyrus and the frontal and parietal neocortex, and lower neuron counts in the hippocampus and basal nucleus of Meynert. Features of the Klüver-Bucy syndrome (range behaviour and hypermetamorphosis) were significantly associated with lower counts of large neurons in the parahippocampal gyrus and parietal neocortex, but not with more severe plaque or tangle formation or with neuronal loss in the subcortical nuclei. No correction was made for multiple comparisons. These findings may signify decreased cortical inhibition in patients with relatively well preserved subcortical structures who show features suggestive of the Klüver-Bucy syndrome. High PAC scores on the SGRS could reflect more advanced and widespread cerebral pathology in the end stages of AD.


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