Neuroendocrinological Function in Alzheimer’s Disease

Franceschi, M.; Perego, L.; Ferini‐Strambi, Luigi; Smirne, S.; Canal, N.

doi:10.1159/000125036

Cited by 23 publications

(8 citation statements)

References 19 publications

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“…In humans a decreased level of (3-endorphin ((3-End)-like-immunoreactivity in cerebrospinal fluid of patients with AD [ 123] and with ATD [124] has been described. This finding was not confirmed in more recent studies [108] and others found increased plasma levels in AD patients [125].…”

Section: ] /}-Endorphincontrasting

confidence: 65%

Neuropeptide Changes in Dementia: Pathogenetic Implications and Diagnostic Value

Valenti¹

1996

Gerontology

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The main object of this review is to describe the most significant alterations of neuropeptide patterns occurring in the brain and in the cerebral spinal fluid of demented patients and particularly of elderly patients with Alzheimer type dementia. The changes in concentration in the different brain areas are described along with their peripheral endocrine implications. Alterations in the synthesis and release of neuropeptides may play a significant role in the pathogenesis of dementia in elderly patients, in addition to the well known changes in classical neurotransmitter systems. Measurements of neuropeptide levels in cerebrospinal fluid or postmortem brain material as alleged biological markers for the diagnostic purpose, however, have produced controversial results. Neuropeptide changes in the demented brain show regional differences and are not specific and selective enough to differentiate between senile dementia, Alzheimer type dementia and other degenerative disorders.

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Section: ] /}-Endorphincontrasting

confidence: 65%

Neuropeptide Changes in Dementia: Pathogenetic Implications and Diagnostic Value

Valenti¹

1996

Gerontology

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“…Indeed, in previous studies basal and post-dexamethasone cortisol levels were found to be higher in DAT patients than in age-matched healthy controls 3, 27100 Pavia, ltalia Accepted for publication December 27, 1989 I (10, 11). Moreover, plasma P-endorphin, whose secretion is directly controlled by CRF, is increased in DAT (12,13).…”

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confidence: 99%

Dementia of the Alzheimer type and hypothalamus-pituitary-adrenocortical axis: changes in cerebrospinal fluid corticotropin releasing factor and plasma cortisol levels

Martignoni

Petraglia

Costa

et al. 2009

Acta Neurologica Scandinavica

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The activity of the hypothalamus‐pituitary‐adrenocortical (HPA) axis was explored in 10 patients with dementia of the Alzheimer type (DAT) and in 11 age‐matched controls, by measuring 1) corticotropin‐releasing factor (CRF) levels in cerebrospinal fluid (CSF), 2) the circadian changes of plasma cortisol, 3) and 4) the plasma cortisol response to dexamethasone suppression test (DST) and to CRF stimulation test. CSF CRF levels in DAT were significantly higher than in controls and inversely related to the Mini Mental State (MMS) score. The patients also displayed increased morning (0800 h) plasma cortisol values, with higher mesor and amplitude in the circadian pattern. Dexamethasone resistance was shown by 6 of the 10 DAT subjects. Plasma cortisol response to CRF administration was similar in the two groups, except for the peak values, which in DAT patients were reached earlier than in controls. The present data suggest an overactivity of HPA axis in DAT; its possible role in the evolution of the disease is discussed.

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“…The opioid peptides are involved in a variety of behavioral and physiological processes such as eating, drinking, reproduction, stress, pain, emotions, learning, and homeostasis (Morley et al, 1983;Ferin and Vande Wiele, 1984;Olson et al, 1990;Dondi et al, 1991;Laatikainen, 1991;Neumann et al, 1992;Russell et al, 1992), and opioid dysfunction has been implicated in several neurological/psychiatric disor- GPi HG IC IN INAH-1 INF IS LH LT LV MB MPA MT NA NBM oc third ventricle amygdala, central (Berger et al, 1981;Franceschi et al, 1986;Seizinger et al, 1986;Berger and Nemeroff, 1987;Cavagnini et al, 1987;Terenius et al, 1987;Franceschi et al, 1988;Chamberlain and Herman, 1990;Zis and Garland, 1991). A number of immunocytochemical and biochemical studies have shown that the peptides are concentrated heavily in the hypothalamus of various species, including humans (Bloch et al, 1978;Gramsch et al, 1979Gramsch et al, , 1982Kubek and Wilber, 1980;Maysinger et al, 1982;Pittius et al, 1983Pittius et al, , 1984Suda et al, 1985).…”

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confidence: 99%

Opioid precursor gene expression in the human hypothalamus

Sukhov

Walker

Rance

et al. 1995

J of Comparative Neurology

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Using in situ hybridization histochemistry, we studied the distribution of neurons that express preproopiomelanocortin (pre-POMC), preprodynorphin (pre-PDYN), and preproenkephalin (pre-PENK) gene transcripts within the human hypothalamus and surrounding structures. Of the three opioid systems, pre-POMC neurons have the most restricted distribution. Pre-POMC cells are most numerous in the infundibular nucleus and retrochiasmatic area of the mediobasal hypothalamus; a few labeled cells are present within the boundaries of the ventromedial nucleus and infundibular stalk. Pre-POMC message was not found in the limited samples of structures adjacent to the hypothalamus. In contrast to neurons that express pre-POMC, neurons expressing pre-PDYN and pre-PENK are more widely represented throughout the hypothalamus and extrahypothalamic structures. However, pre-PDYN and pre-PENK cells differ from one another in distribution. Pre-PDYN message is especially abundant in neurons of the tuberal and mammillary regions, with a distinct population of labeled cells in the premammillary nucleus and dorsal posterior hypothalamus. Pre-PDYN gene expression also is found in neurons of the dorsomedial nucleus, ventromedial nucleus, caudal magnocellular portion of the paraventricular nucleus, dorsolateral supraoptic nucleus, tuberomammillary nucleus, caudal lateral hypothalamus, and retrochiasmatic area. In structures immediately adjacent to the hypothalamus, pre-PDYN neurons were observed in the caudate nucleus, putamen, cortical nucleus of the amygdala, and bed nucleus of the stria terminalis. Pre-PENK neurons occur in varying numbers in all hypothalamic nuclei except the mammillary bodies. The chiasmatic region is particularly rich in pre-PENK neurons, with the highest packing density in the intermediate nucleus [the intermediate nucleus (Braak and Braak [1987] Anat. Embryol. 176:315-330) has also been termed the sexually dimorphic nucleus of the preoptic area (SDA-POA; Swaab and Fliers [1985] Science 228:1112-1115) or the interstitial nucleus of the anterior hypothalamus 1 (Allen et al. [1989] J. Neurosci. 9:497-506)], dorsal suprachiasmatic nucleus, medial preoptic area, and rostral lateral hypothalamic area. Pre-PENK neurons are numerous in the infundibular nucleus, ventromedial nucleus, dorsomedial nucleus, caudal parvicellular portion of the paraventricular nucleus, tuberomammillary nucleus, lateral hypothalamus, and retrochiasmatic area. Only a few lightly labeled cells were found in the periphery of the supraoptic nucleus and lateral tuberal nucleus. In areas adjacent to the hypothalamus, cells that contain pre-PENK message occur in the nucleus basalis of Meynert, central nucleus of amygdala, bed nucleus of the stria terminalis, caudate nucleus, and putamen.(ABSTRACT TRUNCATED AT 400 WORDS)

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Neuroendocrinological Function in Alzheimer’s Disease

Cited by 23 publications

References 19 publications

Neuropeptide Changes in Dementia: Pathogenetic Implications and Diagnostic Value

Neuropeptide Changes in Dementia: Pathogenetic Implications and Diagnostic Value

Dementia of the Alzheimer type and hypothalamus-pituitary-adrenocortical axis: changes in cerebrospinal fluid corticotropin releasing factor and plasma cortisol levels

Opioid precursor gene expression in the human hypothalamus

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