Evolution of Alzheimer's disease-related cytoskeletal changes in the basal nucleus of Meynert

2000 ◽  
Vol 100 (3) ◽  
pp. 259-269 ◽  
Author(s):  
I. Sassin ◽  
C. Schultz ◽  
D. R. Thal ◽  
U. Rüb ◽  
K. Arai ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Basal Nucleus ◽  
Basal Nucleus Of Meynert

Clinical and neuropathological correlates of depression in Alzheimer's disease

1992 ◽  
Vol 22 (4) ◽  
pp. 877-884 ◽  
Author(s):  
Hans Förstl ◽  
Alistair Burns ◽  
Philip Luthert ◽  
Nigel Cairns ◽  
Peter Lantos ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cognitive Impairment ◽  
Age Of Onset ◽  
Neuronal Degeneration ◽  
Cholinergic Neurons ◽  
Organic Substrate ◽  
Basal Nucleus ◽  
Alzheimer Pathology ◽  
Basal Nucleus Of Meynert

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.

Correlative decrease of large neurons in the neostriatum and basal nucleus of Meynert in Alzheimer's disease

1989 ◽  
Vol 504 (2) ◽  
pp. 354-357 ◽  
Author(s):  
Kiyomitsu Oyanagi ◽  
Hitoshi Takahashi ◽  
Koichi Wakabayashi ◽  
Fusahiro Ikuta
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Basal Nucleus ◽  
Basal Nucleus Of Meynert ◽  
Large Neurons

scholarly journals Morphofunctional Changes and Compensatory Mechanisms in the Human Brain with Aging and in Alzheimer's Disease

2020 ◽  
Vol 9 (1) ◽  
pp. 77-85
Author(s):  
T. A. Ishunina ◽  
I. N. Bogolepova ◽  
D. F. Swaab
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Human Brain ◽  
Metabolic Activity ◽  
Brain Structures ◽  
Female Group ◽  
Compensatory Mechanisms ◽  
Basal Nucleus ◽  
Age Related ◽  
Adaptive Mechanisms

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.

Neuropathological Correlates of Behavioural Disturbance in Confirmed Alzheimer's Disease

1993 ◽  
Vol 163 (3) ◽  
pp. 364-368 ◽  
Author(s):  
Hans Förstl ◽  
Alistair Burns ◽  
Raymond Levy ◽  
Nigel Cairns ◽  
Philip Luthert ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Rating Scale ◽  
Neuronal Loss ◽  
Cortical Inhibition ◽  
Parahippocampal Gyrus ◽  
Subcortical Structures ◽  
Behavioural Disturbance ◽  
Basal Nucleus ◽  
A Prospective Study

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.

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.

scholarly journals Anatomic survey of seeding in Alzheimer’s disease brains reveals unexpected patterns

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Barbara E. Stopschinski ◽  
Kelly Del Tredici ◽  
Sandi-Jo Estill-Terpack ◽  
Estifanos Ghebremdehin ◽  
Fang F. Yu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurofibrillary Tangle ◽  
Internal Capsule ◽  
Brain Regions ◽  
Progressive Increase ◽  
Substantia Nigra Pars Compacta ◽  
Basal Nucleus ◽  
Tau Aggregation ◽  
Analytical Tools

AbstractTauopathies are heterogeneous neurodegenerative diseases defined by progressive brain accumulation of tau aggregates. The most common tauopathy, sporadic Alzheimer’s disease (AD), involves progressive tau deposition that can be divided into specific stages of neurofibrillary tangle pathology. This classification is consistent with experimental data which suggests that network-based propagation is mediated by cell–cell transfer of tau “seeds”, or assemblies, that serve as templates for their own replication. Until now, seeding assays of AD brain have largely been limited to areas previously defined by NFT pathology. We now expand this work to additional regions. We selected 20 individuals with AD pathology of NFT stages I, III, and V. We stained and classified 25 brain regions in each using the anti-phospho-tau monoclonal antibody AT8. We measured tau seeding in each of the 500 samples using a cell-based tau “biosensor” assay in which induction of intracellular tau aggregation is mediated by exogenous tau assemblies. We observed a progressive increase in tau seeding according to NFT stage. Seeding frequently preceded NFT pathology, e.g., in the basolateral subnucleus of the amygdala and the substantia nigra, pars compacta. We observed seeding in brain regions not previously known to develop tau pathology, e.g., the globus pallidus and internal capsule, where AT8 staining revealed mainly axonal accumulation of tau. AT8 staining in brain regions identified because of tau seeding also revealed pathology in a previously undescribed cell type: Bergmann glia of the cerebellar cortex. We also detected tau seeding in brain regions not previously examined, e.g., the intermediate reticular zone, dorsal raphe nucleus, amygdala, basal nucleus of Meynert, and olfactory bulb. In conclusion, tau histopathology and seeding are complementary analytical tools. Tau seeding assays reveal pathology in the absence of AT8 signal in some instances, and previously unrecognized sites of tau deposition. The variation in sites of seeding between individuals could underlie differences in the clinical presentation and course of AD.

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