The amygdala in Alzheimer's disease: Neuropathology and Alz 50 Immunoreactivity

Unger, J.; Lapham, Lowell W.; McNeill, Thomas H.; Eskin, Thomas A.; Hamill, RW

doi:10.1016/0197-4580(91)90063-p

Cited by 55 publications

(29 citation statements)

References 61 publications

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“…The Am is deeply involved in several severe neurologic and psychiatric diseases, such as Alzheimer' disease and related neurodegenerative diseases (Brockhaus 1938;Herzog and Kemper 1980;Unger et al 1988Unger et al , 1991Brady and Mufson 1990;Esiri et al 1990Esiri et al , 1997Emre et al 1993;Kromer Vogt et al 1990;Braak and Braak 1991;Mann 1992;Benzing et al 1993;Vereecken et al 1994;Braak et al 1996;Schmidt et al 1996;Jellinger and Bancher 1998;Chow and Cummings 2000;ShibuyaTayoshi et al 2005), in Huntington's chorea (Zech et al 1986;Mann et al 1993;Rosas et al 2003), in temporal lobe epilepsy (Bruton 1988;Feindel and Rasmussen 1991;Gloor 1992;Hudson et al 1993;Honavar and Meldrum 1997;Wolf et al 1997;Pitka¨nen et al 1998;Thom et al 1999;Aliashkevich et al 2003;Pitka¨nen 2004), in schizophrenia (Bogerts 1993;Bogerts et al 1993;Roberts et al 1997;Shenton et al 2001), in bipolar disorder (Haldane and Frangou 2004), and in autism (Amaral et al 2003;Kemper 2003, 2005).…”

Section: Nitrergic Neurons Of the Am In Physiology And Pathologymentioning

confidence: 99%

Nitric oxide synthase-containing neurons in the amygdaloid nuclear complex of the rat

et al. 2006

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The nitric oxide-producing neurons in the rat amygdala (Am) were studied, using reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) histochemistry. Almost all nuclei of the Am contained NADPHd-positive neurons and fibers, but the somatodendritic morphology and the intensity of staining of different subpopulations varied. The strongly stained neurons displayed labeling of the perikaryon and the dendritic tree with Golgi impregnation-like quality, whilst the dendrites of the lightly stained neurons were less successfully followed. Many strongly positive neurons were located in the external capsule and within the intraamygdaloid fiber bundles. A large number of small, strongly stained cells was present in the amygdalostriatal transition area. In the Am proper, a condensation of deeply stained cells occurred in the lateral amygdaloid nucleus. In the basolateral nucleus, the strongly NADPHd-positive neurons were few, and were located mainly along the lateral border of the nucleus. These cells clearly differed from the large, pyramidal, and efferent cells. The basomedial nucleus contained numerous positive cells but most of them were only lightly labeled. A moderate number of strongly stained neurons appeared in the medial division of the central nucleus, and a larger accumulation of strongly positive cells was present in the lateral and the capsular divisions. The medial amygdaloid nucleus contained numerous moderately stained neurons and displayed the strongest diffuse neuropil staining in Am. In the nucleus of the lateral olfactory tract, the first layer contained only NADPHd-stained axons, in the second layer, there were numerous moderately stained cells, and in the third layer, a few but deeply stained neurons. From the cortical nuclei, the most appreciable number of stained neurons was seen in the anterior cortical nucleus. The anterior amygdaloid area contained numerous NADPHd-positive neurons; in its dorsal part the majority of cells were only moderately stained, whereas in the ventral part the neurons were very strongly stained. The intercalated amygdaloid nucleus lacked NADPHd-positive neurons but an appreciable plexus of fine, tortuous axons was present. In the intra-amygdaloid part of the bed nucleus of the stria terminalis (st) some lightly stained cells were seen but along the entire course of st strongly stained neurons were observed. Some Am nuclei, and especially the central lateral nucleus and the intercalated nucleus, display considerable species differences when compared with the primate Am. The age-related changes of the nitrergic Am neurons, as well as their involvement in neurodegenerative diseases is discussed.

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Section: Nitrergic Neurons Of the Am In Physiology And Pathologymentioning

confidence: 99%

Nitric oxide synthase-containing neurons in the amygdaloid nuclear complex of the rat

et al. 2006

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“…Although brain areas belonging to the olfactory system are consistently affected during the neurodegenerative process, i.e. plaques, NFTs and cell loss in the olfactory bulb, olfactory nuclei and amygdala [16][17][18], it is presently unknown at what stage during the disease pathological neuronal changes spread to the peripheral olfactory epithelium and related nerve fibres. Using a panel of highly specific monoclonal antibodies, we were unable to detect the presence of Ù or ß-amyloid in olfactory mucosa in any of the 5 AD patients with beginning dementia.…”

Section: Discussionmentioning

confidence: 99%

Histological Markers in Nasal Mucosa of Patients with Alzheimer’s Disease

Höck¹,

Golombowski²,

Müller‐Spahn³

et al. 1998

Eur Neurol

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Neuropathological changes such as dystrophic neurites and the presence of abnormal τ protein in the olfactory system, including primary sensory cells and nerve fibres have previously been demonstrated in nasal mucosa tissue of patients with Alzheimer’s disease (AD). These changes were detected in autopsy-derived material from histopathologically confirmed AD cases as well as in biopsy tissue from clinical severely ill AD patients. To investigate the potential usefulness for the early diagnosis of AD, we obtained biopsy tissue from olfactory mucosa from 5 clinically mild to moderate AD patients and stained for the presence of τ or β-amyloid by immunocytochemistry using a panel of specific antibodies. No positive staining was found in any of the cases. For comparison, post-mortem olfactory tissue from AD patients with severe neuropathological changes (widespread neurofibrillary tangles and amyloid in the brain) was investigated. In these severe cases, τ immunoreactivity was found in fine nerve fibres in the lamina propria and in a few olfactory epithelial cells. These results are consistent with other reports showing that cytoskeletal changes and τ pathology in the olfactory epithelium are not primary (or specific) features of AD and may occur predominantly in late stages of the disease.

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“…Apart from β-amyloid precursor protein synthesis, activated glial cells might be involved in processing and phagocytosis of the β-amyloid protein in senile plaques [Ishii et al, 1989;Itagaki et al, 1989;Yamaguchi et al, 1992;Akiyama, 1994;el Hachimi and Foncin, 1994]. The distribution pattern of neuritic plaques in the amygdala is well known in Alzheimer's disease [Jamada and Mehraein, 1968;Brashear et al, 1988;Kromer-Vogt et al, 1990;Unger et al, 1991;Benzing et al, 1993]. However, initial Alzheimer-related changes have only been regarded by few investigators [Mann et al, 1988].…”

Section: Discussionmentioning

confidence: 99%

“…The amygdala is severely affected in Alzheimer's disease and particularly rich in neuritic plaques [Jamada and Mehraein, 1968;Brashear et al, 1988;Kromer-Vogt et al, 1990;Mann et al, 1990;Scott et al, 1991;Unger et al, 1991;Scott et al, 1992;Benzing et al, 1993;Vereecken et al, 1994;Yilmazer et al, 1995;Braak et al, 1996]. The nuclear complex has three major divisions.…”

Section: Introductionmentioning

confidence: 99%

Alzheimer’s Disease

Yilmazer-Hanke¹

1998

Cells Tissues Organs

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The gradual development of Alzheimer-related neurofibrillary changes and β-amyloid deposits have been investigated in the amygdala and cerebral cortex with advanced silver methods. Neurofibrillary tangles occur within the somata of nerve cells, while neuropil threads are located in nerve cell processes. In neuritic plaques, there are both neuronal processes containing neurofibrillary changes and extracellular deposits of β-amyloid protein. The amygdala early displays Alzheimer-type pathology and is typically rich in neuritic plaques. Neuritic plaques do not occur in the amygdala in the absence of neuropil threads and neurofibrillary tangles in the entorhinal region and amygdala. In contrast to the gradual increase in the number of neurofibrillary tangles and neuropil threads, neuritic plaques grow in size and number along with advancement in the neurofibrillary and β-amyloid pathology. The findings indicate that neuropil threads and neurofibrillary tangles in the entorhinal region and amygdala precede neuritic plaques in the amygdala, and the density of neuritic plaques is related both to the degree of neurofibrillary and β-amyloid pathology in the cerebral cortex.

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The amygdala in Alzheimer's disease: Neuropathology and Alz 50 Immunoreactivity

Cited by 55 publications

References 61 publications

Nitric oxide synthase-containing neurons in the amygdaloid nuclear complex of the rat

Nitric oxide synthase-containing neurons in the amygdaloid nuclear complex of the rat

Histological Markers in Nasal Mucosa of Patients with Alzheimer’s Disease

Alzheimer’s Disease

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