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[QUOTE]Originally posted by Quetzalcoatl: [QB] [QUOTE]Originally posted by Tukuler: [qb] Small class student observation Quetz' lecture is polemic thus subjectively flawed. He chides Finch MD should know albinos cannot produce eumelanin, a straw man unless quoting Finch saying albinos have melanin. Not being an MD, Quetz doesn't know any better that OCA1B albinos can have eumelanin (source withheld until Quetz recants). [/qb][/QUOTE]The problem is that all this “albino” hype is worthless. Albinos have normal amounts of neuromelanin (the melanin in the brain) equal to that of as. As a matter of fact, since amounts of neuromelanin increase with age, an old albino will have [b]more neuromelanin than a young black person[/b] Parkinson Disease at an Early Age by Juan Sanchez-Ramos- [b]Medical Director of the National Parkinson Foundation[/b], Professor of Neurology at the University of Miami, Miami, FL [URL] http://www.martinpurchase.org.uk/downloads/ParkinsonDiseaseatanEarlyA [/URL] [QUOTE]Pigment (neuromelanin) is formed within nigral cells as a by-product of dopamine metabolism. [b]Neuromelanin differs from skin pigment. Caucasians, Africans, Orientals and albinos have equal amounts of neuromelanin.[/b] Neuromelanin is absent @ birth-in all people. It accumulates after birth. And, In most people, the nigral cells are fully pigmented @ age 16 years.[/QUOTE]Robins, AH (1991) [b]Biological Perspectives in Human Pigmentation[/b]. Cambridge: Cambridge Univ. Press [QUOTE] p. 81-82 The genesis of neuromelanin bears no similarity to the development of the melanosomes within the melanocytes. Its concentration in the brain is proportional to the age of the individual, and is[b] totally independent of ethnic pigmentation.[/b][/QUOTE]Foley JM, Baxter D. 1958 “On the nature of pigment granules in the cell of the locus coeruleus and substantia nigra,” [b]J Neuropathol Exp Neurol[/b] 17:586–598. Zecca, L. et al. 2001 “Substantia nigra neuromelanin: structure, synthesis, and molecular behaviour,” [b]J Clin Pathol:Mol Pathol[/b] 54:414–418 [QUOTE]Abstract The pigmented neurones of the substantia nigra are typically lost in Parkinson’s disease; however, the possible relation between neuronal vulnerability and the presence of neuromelanin has not been elucidated. Early histological studies revealed the presence of increasing amounts of neuromelanin in the substantia nigra with aging in higher mammals, showed that the neuromelanin granules are surrounded by a membrane, and comparatively evaluated the pigmentation of the substantia nigra in different animal species. Histochemical studies showed the association of neuromelanin with lipofuscins. However, systematic investigations of the structure, synthesis, and molecular interactions of neuromelanin have been undertaken only during the past decade. In these later studies, neuromelanin was identified as a genuine melanin with a strong chelating ability for iron and an affinity for compounds such as lipids, pesticides, and MPP+. The affinity of neuromelanin for a variety of inorganic an organic toxins is consistent with a postulated protective function for neuromelanin. Moreover, the neuronal accumulation of neuromelanin during aging and the link between its synthesis and a high cytosolic concentration of catechols suggest a protective role. However, its putative neuroprotective effects could be quenched in conditions of toxin overload. However, tyrosinase has not been detected in the substantia nigra by immunohistochemistry.41 [b]Moreover, albinos who lack tyrosinase display normally pigmented substantia nigra[/b].10[/QUOTE]Zecca, L., et al. 2003 “Neuromelanin of the substantia nigra: a neuronal black hole with protective and toxic characteristics,” [b]TRENDS in Neurosciences [/b]26(11): 578-580 {QUOTE][b]Albinos that lack tyrosinase, however, have a normally pigmented substantia nigra [17].[/b] . . . Recently, NM synthesis was experimentally induced in cultured rat substantia nigra neurons exposed to L-dopa [21]. This model reproduced nigral NM in that the chemical structure as measured by electron-spin resonance [b]was identical to human NM,[/b] and the pigment was localized in the characteristic organelles surrounded by double membrane. Neuromelanin accumulates normally with age in human, rat, canine and primate substantiae nigrae [32]. In humans, the first NM granules appear around the third year of life [33] and NM concentrations in the substantia nigra increase linearly over aging, reaching values as high as 4.0 mg g21 in those aged in their eighties.[/QUOTE] Zucca, F.A., et al. 2004 “The Neuromelanin of Human Substantia Nigra: Physiological and Pathogenic Aspects,” [b]Pigment Cell Res.[/b] 17: 610–617. [QUOTE]Neuromelanin (NM) accumulates as a function of age in normal human substantia nigra (SN) but is relatively depleted in the SN of patients with Parkinson disease (PD). Moreover, albinos (who lack functional tyrosinase) display normally pigmented neurons in the SN (38).[/QUOTE]Zucca, F. A., et al. 2013 “Neuromelanin of the Human Substantia Nigra: An Update,” [b]Neurotox Res[/b] DOI 10.1007/s12640-013-9435-y [QUOTE] Dopaminergic neurons of the substantia nigra selectively degenerate over the course of Parkinson’s disease. These neurons are also the most heavily pigmented cells of the brain, accumulating the dark pigment neuromelanin over a lifetime. The massive presence of neuromelanin in these brain areas has long been suspected as a key factor involved in the selective vulnerability of neurons. [b]Furthermore, a normal content of NM [neuromelanin] is present in SN of albinos which lack functional tyrosinase[/b] (Foley and Baxter 1958 ). Other enzymes than tyrosinase might be involved in NM synthesis, but so far a neuron specific enzymatic synthesis pathway has not been unequivocally demonstrated.[/QUOTE] [/QB][/QUOTE]
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