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Biomedical subjects

J Constantinidis

Publications and source records attributed to J Constantinidis.

156 records · Page 9Linked to original sources
PubMedDate not supplied

[Alzheimer's disease and the zinc theory].

UNLABELLED: In Alzheimer's disease, the Primum Movens is amyloid production on precapillaries: dysphoric angiopathy, and capillaries: senile plaques. Cerebral amyloid alone may be asymptomatic. Clinical symptoms of amnesia appear when amyloid induces neighbouring neuritic alterations: paired helical filaments and distant neuronal body lesions: neurofibrillary tangles. HYPOTHESIS: the amyloid induces zinc deficiency which produces the tangles. In Alzheimer's disease, cerebral zinc decreases particularly in the hippocampus. Without amyloid, neurofibrillary tangles are produced by metalotoxicity and therefore probably brain zinc displacement: by lead: encephalopatia saturnica, by calcium deficiency: Guam's encephalopathy, by aluminium, by blood-brain-barrier disturbances probably leading to an abnormal entry of metals in the brain (dementia pugilistica, viral encephalitides). Neurofibrillary tangles may be produced by deficiency of the following zinc enzymes: 1) those of DNA metabolism inducing abnormal DNA and therefore abnormal protein synthesis: paired helical filaments and neurofibrillary tangles; 2) of glutamate-dehydrogenase resulting in an excitotoxic increase of glutamate, which may produce neurofibrillary tangles, particularly in the hippocampus rich in glutamate pathways; 3) those of neuronal detoxication: superoxide-dismutase, carbonic anhydrase, lactate-dehydrogenase leading to neuronal toxicity particularly in the hippocampus normally rich in superoxide dismutase; 4) those of neurotransmitters metabolisms (opioid peptides, GABA, acetylcholine). Therapeutic implication: a non-toxic zinc complex crossing the Blood-Brain-Barrier should be useful.

Adult↗
PubMedDate not supplied

Immunohistochemical mapping of delta sleep-inducing peptide in the cat brain and hypophysis. Relationships with the LHRH system and corticotropes.

Using the indirect immunofluorescence method, the distribution of the delta sleep-inducing peptide was studied in the cat brain and hypophysis. Delta sleep-inducing peptide-like-immunoreactive cell bodies mostly visualized in colchicine-pretreated animals were mainly found scattered throughout the diagonal band of Broca, the ventral septum and the anterior hypothalamic areas. A few immunoreactive cell somata were also seen in the ventrolateral hypothalamic area and more occasionally in the triangular septal nucleus. The heaviest concentrations of delta sleep-inducing peptide-like-immunoreactive varicose fibres and terminal-like structures were observed in the septo-preoptic region, in the median eminence and pituitary stalk. Some other brain regions supplied with few delta sleep-inducing peptide-immunoreactive fibres included the fimbria-fornix, the dorsal part of the subfornical organ, the medial habenular nucleus and more caudally, the periaqueductal gray. Elution-restaining experiments revealed that delta sleep-inducing peptide-like immunoreactivity frequently occurred in luteinizing hormone-releasing hormone-immunoreactive neurons and vice versa. At the pituitary level, delta sleep-inducing peptide-like immunoreactivity was detected in most, if not all, melanocorticotropes of the pars intermedia and further in a large subpopulation of corticotropes mainly located in the zona tuberalis of the pars distalis. Taken together these anatomical findings support the view that delta sleep-inducing peptide (or a closely related molecular form) could play a modulatory role at various levels of the hypothalamo-pituitary system.

Animals↗
PubMedDate not supplied

[A familial syndrome: a combination of Pick's disease and amyotrophic lateral sclerosis].

The association of Pick's Disease (PD) and Amyotrophic Lateral Sclerosis (ALS) as a familial syndrome is reported for the first time. Four members in two generations of the investigated family suffered from this syndrome, allowing the hypothesis of a dominant mode of inheritance. PD is primary, with onset at 58 to 67 years: loss of interests, depression, aggressivity, perseveration , stereotypies, reduction of speech until total mutism; a few months later appear ALS signs: fasciculations and/or pyramidal symptoms. The total evolution is 3 to 5 years. The brain showed a fronto-temporal atrophy spreading to the precentral gyrus with cortical and white matter gliosis, neuronal loss, atrophic neurons and some ballooned cells, but without senile plaques (SP), neurofibrillary tangles (NFT) or cortical spongiosis; the spinal cord and the medulla oblongata showed typical ALS lesions; mild lesions in the basal nuclei, particularly in the substantia nigra and the pallidum. The differential diagnosis is discussed with: Alzheimer's Disease + ALS (SP + NFT); the Guam syndrome (NFT); Creutzfeldt-Jakob's Disease (cortical microspongiosis); ALS + dementia (primary ALS); Mitsuyama's syndrome (primary dementia and secondary ALS, but with cortical spongiosis and without familial incidence).

Amyotrophic Lateral Sclerosis↗