Food Causing Dementia,
In Short :
Due to heat, new substances originate in especially proteinous prepared foods. Part of these substances are mutagenic or toxic. And some of these can also bind to neurotransmitter-receptors and -transporters in the brain. Because of the mutagenic properties of these substances,
neurotransmitter-receptors and / or -transporters are destroyed. Depending on what kind of neurotransmitter is destroyed, different brain diseases can be caused, like dementia, Parkinson's and schizophrenia.
To stop progress of, or
prevent brain diseases, consume as little prepared food (proteinous prepared
food in particular). (See
diet suggestions) Consume as much fruits (there are about 6000 different
fruits), and some fresh raw animal food regularly (like sashimi or fresh raw
egg yolk, requiring an hour rest to digest by the way!). Combined, these foods contain
all nutrients you need.
Not at all if you eat fresh
raw foods regularly.
When we are
old, we are supposed to be wiser, and advise the younger.
When we are
old, we are not supposed to wear a diaper and forget our grandchildren's names.
In Detail :
The brain processes
signals ; signals from the eyes, ears, skin, etc. These signals are transmitted
in the brain by messengers or neurotransmitters. These neurotransmitters can
only function if there is something they can deliver the messages to, i.e., receptors.
In brain-diseases production or secretion of one or more neurotransmitters is malfunctioning, or receptors have been destroyed. Depending on which
neurotransmitter-system is failing, a brain-disease is caused.
Parkinsonís dopamine- (1) and / or serotonine-
are deficient. (2) In dementia acetylcholine-
metabolism is impaired. And in schizophrenia in general too little dopamine (3) and / or serotonine (4) reach the receptors.
What causes brain-diseases ?
receptors, or structurally
or secretion of neurotransmitters cause brain diseases.
Prepared food, and proteinous†prepared food in
particular always contains such substances ; due to the influence of heat, in
all foods that are cooked, steamed, baked, grilled etc., new substances originate, like beta-carbolines, pyridines,
quinolines and other heterocyclic amines. (see this
- †† Some
of these substances are directly toxic to the brain. (5)
these substances only become toxic (or more toxic) through being partly
in the body (6), by enzymes (7) or by oxidation. (8)
Sometimes these substances are toxic
because they decrease, sometimes irreversibly (9), neurotransmitter levels
(10). Some of these substances are only toxic to a single type of
neurotransmitter receptors, like dopamine receptors. (11)
- †† To
function, receptors are not just susceptible to neurotransmitters made by the
but also to substances that look alike, disturbing the normal influence of
That's why drugs fighting the symptoms of brain-diseases
temporarily can have some effects. Many
beta-carbolines, for example, stimulate secretion of acetylcholine. Eventually this may lead to
exhaustion of the acetylcholine-system, and dementia.
-††† Neurotransmitter-transporters can also be
''occupied'' by substances that look like neurotransmitters. Certain
beta-carbolines and quinolines for example, can ''occupy''
dopamine-transporters, which can also cause Parkinsonís. (12) Because
when dopamine receptors are occupied, dopamine accumulates, and more likely
- †† Also, many beta-carbolines locally stimulate
secretion of glutamate (a neurotransmitter), by stimulating secretion of
acetylcholine (13), like amphetamines and cocaine do.
Secretion of too much glutamate locally damages the brain (15), by
secretion of radicals. (16)
Glutamate also stimulates secretion
and decomposition of dopamine (17), causing exhaustion, and eventually
death of dopamine-receptors (18). Dopamine receptors are deficient in
Parkinsonís. Logically, this can lead to schizophrenia too. (19)
(like cocaine can (20)) It just takes a little time. That's why
Ďnon-environmentalí schizophrenia mostly is not 'discovered' before the age of
15 to 25.
In only 10 to
20% of patients Alzheimerís is inherited.
about the rest ?
Acetylcholine is needed
to think. In Alzheimerís acetylcholine metabolism is impaired, causing severe
memory lapses. At the onset of Alzheimers acetylcholine deficiency remains unnoticed,
due to increased activity of remaining receptors. In advanced Alzheimerís remaining
receptors cannot compensate the loss of receptors anymore. (21)
can be killed by inactive substances that occupy receptors and look similar to
neurotransmitters. (22) In Alzheimerís, receptors are occupied by a plague of damaged proteins and -fats (23) and brain fluids contain
higher levels of these substances. (24) In Alzheimerís, the body tries
to eliminate those substances by increasing the level of 'cleaners'. (25)
Some of those cleaners can however also damage brain-neurons. (26)
in Alzheimerís is not caused by a genetic failure that causes enzymes to
decompose acetylcholine too fast; in Alzheimerís, activity of
acetylcholine-decomposing enzymes is not increased, but even decreased 24% (18%
in Parkinsonís)(27). This indicates that production / secretion of
acetylcholine is exhausted. And yet substances inhibiting this enzyme are used
as anti-Alzheimer 'drugs' (28), just to fight symptoms. Production of acetylcholine can be
exhausted through ongoing stimulation of acetylcholine-secretion by
beta-carbolines from prepared food in the first place.
In Alzheimerís even in
broad daylight serotonine is transformed into melatonine, which isn't normal. (29)
Therefore, dementia (and Parkinsonís) often comes with depressions. (30)
Beta-carbolines from cooked foods can
impair the serotinine-melatonine metabolism.
Acetylcholine is also
needed for muscle-contractions. Normally, secretion of acetylcholine is
regulated by dopamine. In Parkinsonís however, dopamine-receptors
have been damaged, or occupied by dietary protein-oxidation products.
Therefore, in Parkinsonís muscle-contractions can not be controlled as well.
Whether you will get
Parkinsonís, depends on how sensitive your receptors are. (31)
amines and imidazoles damage dopamine molecules, causing reactive radicals to
originate. (32) These radicals damage DNA (33) and kill brain
cells. (34) Too much iron (34), copper or manganese (35)
can also cause dopamine to oxidize.
In Parkinsonís patients
radicals levels are elevated, and antioxidant levels are decreased. (36) In
Parkinsonís CRF-level is decreased too. And certain pyridines that are toxic to
dopamine-receptors, also decrease CRF level. (37) Those
pyridines too originate from food-proteins, due to the influence of heat.
Many beta-carbolines influence
the secretion and decomposition of dopamine (38). Blood-beta-carboline- (39)
,brainfluid-beta-carboline- (40) and / or -toxic quinoline level (41)
are elevated in Parkinson's patients.
Some schizophrenics are
born that way, and others become schizophrenic in reaction to rape or other
excessive psychological stress. Some just get 'unreal' signals from prepared
dopamine-receptors are more sensitive. (42)
Wheat-opioid peptides can
occupy dopamine-receptors, what
may cause schizophrenia. In areas
where people hardly consume wheat-products, schizophrenia incidence is much
be caused by substances ''occupying'' glutamate-receptors (44), and may also
cause schizophrenia. (45) Certain beta-carbolines /
heterocyclic amines can lower the susceptibility of GABA-receptors (46), and
can therefore cause schizophrenia. (47)
Besides the afore-mentioned
neurotransmitter-receptors, schizophrenia can also be caused through blockage
of glycine- (48) ,N-acetyl aspartate-, phosphatidylcholine- or
Because your brain is the
control-room of your body, blockage of neurotransmitter-receptors can cause all
kinds of psychological and physical problems. Blockage of histamine-,
acetylcholine- or epinephrine-neurotransmitters by anti-depressants for
example, can also cause obesity,
constipation and dizziness (50).
© 2000-2006 Copyright Artists Cooperative Groove Union U.A.
Home + navigation bar:
or without frames:
(1) Mandir, A.S. et al, Poly(ADP-ribose) polymerase activation mediates 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced parkinsonism. Proc.Natl. Acad. Sci. U.S.A. 1999 / 96 (10) / 5774-5779.
(2) Heinz, A. et al, Psychomotor slowing, negative symptoms and dopamine receptor availability - an IBZM SPECT study in neuroleptic-treated and drug-free schizophrenic patients. Schizophr. Res. 1998 / 31 (1) / 19-26. , Moser, A. et al, Salsolinol, catecholamine metabolites, and visual hallucinations in L-dopa treated patients with Parkinson's disease. J. Neural Transm. 1996 / 103 (4)/ 421-432. , Calne, D.B., Treatment of Parkinson's disease, N. Engl.J.Med. 1993 / 329 / 1021.
(3) Witkin, J.M. et al, Behavioural, toxic, and neurochemical effects of sydnocarb, a novel psychomotor stimulant : comparisons with methamphetamine. J. Pharmacol. Exp. Ther. 1999 / 288 (3) / 1298-1310. , Heinz, A. et al, Psychomotor slowing, negative symptoms and dopamine receptor availability - an IBZM SPECT study in neuroleptic-treated and drug-free schizophrenic patients. Schizophr. Res. 1998 / 31 (1) / 19-26. , Meador-Woodruff, J.H. et al, Dopamine receptor transcriptexpression in stratum and prefrontal and occipital cortex. Focal abnormalities in orbitofrontal cortex in schizophrenia. Arch. Gen. Psychiatry 1997 / 54 (12) / 1089-1095. , Ferre, S. Adenosine-dopamine interactions in the ventral striatum. Implications for the treatment of schizophrenia. Psychopharmacology (Berl.) 1997 / 133 (2) / 107-120. , Kuable, M.B. et al, Dopamine, the prefrontal cortex and schizophrenia. J. Psychopharmacol. 1997 / 11 (2) / 123-131.
(4) Otsuki, S. et al, Neurochemical studies of schizophrenia in Japan. Psychiatry Clin. Neurosci. 1997 / 51 (6) / 347-356.
(5) Matsubara, K. et al, Endogenously occurring beta-carboline induces parkinsonism in non primate animals : a possible causative protoxin in idiopathic Parkinson's Disease. J. Neurochem. 1998 / 70 (2) / 727-735. , Dodel, R.C. et al, Caspase-3-like proteases and 6-hydroxydopamine-induced neuronal cell death. Brain. Res. Mol. Brain. Res. 1999 / 64 (1) / 141-148. , Double, K.L. et al, In vitro studies of ferritin iron release and neurotoxicity. J. Neurochem. 1998 / 70 (6) / 2492-2499. , Naoi, M. et al, Oxidation of N-Methyl(R)Salsolinol : involvement to neurotoxicity and neuroprotection by endogenous catechol isoquinolines. J.Neurol. Transm. Suppl. 1998 / 52 / 125-138. , Soto-Otero, R. et al, Studies on interaction between 1,2,3,4-tetrahydro-beta-carboline and cigarette smoke : a potential mechanism of neuroprotection for Parkinson's disease. Brain Res. 1998 / 802(1-2) / 155-162. , Nagatsu, Isoquinoline neurotoxics in the brain and Parkinson's disease. Neurosci. Res. 1997 / 29 (2) / 99-111. , Malgrange, B. et al, beta-Carbolines induce apoptotic death of cerebellar granule neurones in culture. Neuroreport 1996 / 7 (18) / 3041-3045. , Naoi, M. et al, Dopamine-derived endogenous 1(R), 2(N)-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, N-methyl-(R)-salsolinol, induced parkinsonism in rat : biochemical ,pathological and behavioral studies. Brain. Res. 1996 / 709 (2) / 285-295. , Naoi, M. et al, Enzymatic oxidation of the dopaminergic neurotoxin 1(R), 2(N)-dimethyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline, into 1,2(N)-dimethyl-6,7-dihydroxyisoquinolinium ion. Life Sci. 1995 / 57 (11) / 1061-1066. , Maruyama, W. et al, N-methyl(R)salsolinol produces hydroxyl radicals : involvement to neurotoxicity. Free Radic. Biol. Med. 1995 / 19 (1) / 67-75. , McNaught, K.S. et al, Inhibition of complex 1 by isoquinoline derivates structurally related to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Biochem. Pharmacol. 1995 / 50 (11) / 1903-1911. , Skaper, S.D. et al, Characterization of 2,3,4-trihydroxyphenylalanine neurotoxicity in vitro and protective effects of ganglioside GM1 : implications for Parkinson's disease. J. Pharmacol. Exp. ther. 1992 / 263 (3) / 1440-1446. , Naoi, M. et al, Uptake of heterocyclic amines, Trp-P-1 and Trp-P-2, into clonal rat pheochromocytoma PC12h cells by dopamine uptake system. Neurosci. Lett. 1989 / 99 (3) / 317-322. , Rollema, H. et al, In vivo dopaminergic neurotoxicity of the 2-beta-methylcarbolinium ion, a potential endogenous MPP+ analog. Eur. J. Pharmacol. 1988 / 153 (1) / 131-134. , Perry, T.L. et al, 4-Phenylpyridine and three other analogues of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine lack dopaminergic nigrostriatal neurotoxicity in mice and marmosets. Neurosci. Lett. 1987 / 75 (1) / 65-70.
(6) Harik, S.I. et al, On the mechanisms underlying 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine neurotoxicity : the effect of perinigral infusion of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, its metabolite and their analogues in the rat. J. Pharmacol. Exp. ther. 1987 / 241 (2) / 669-676. , Irwin, I. et al, Selective accumulation of MPP+ in the substantia nigra : a key to neurotoxicity ? Life Sci. 1985 / 36 (3) / 207-212. , Heikkila, R.E. et al, Dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse : relationships between monoamine oxidase, MPTP metabolism and neurotoxicity. Life Sci. 1985 / 36 (3) / 231-236. , Melamed, E. et al, Mesolimbic dopaminergic neurons are not spared by MPTP neurotoxicity in mice. Eur. J. Pharmacol. 1985 / 114 (1) / 97-100. , Cohen, G. et al, Pargyline and deprenyl prevent the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in monkeys. Eur. J. Pharmacol. 1984 / 106 (1) / 209-210. , Markey, S.P. et al, Intraneuronal generation of a pyridinium metabolite may cause drug-induced parkinsonism. Nature 1984 / 311 (5985) / 464-467. , Burns, R.S. et al, The neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the monkey and man. Can. J. Neurol. Sci. 1984 / 11 (1 suppl.) / 166-168. , Javitch, J.A. et al, Parkinsononism-inducing neurotoxin, N-methyl-4-phenyl-1,2,3,6-pyridine : characterization and localization of receptor binding in sites in rat and human brain. Proc. Natl. Acad. Sci. U.S.A. 1984 / 81 (14) / 4591-4595. , Hallman, H. et al, Neurotoxicity of the meperidine analogue N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine on brain catecholamine neurons in the mouse. Eur. J. Pharmacol. 1984 / 97 (1-2) / 133-136.
(7) Matsubara, K. et al, Metabolic activation of azaheterocyclics induced dopaminergic toxicity : possible candidate neurotoxins underlying idiopathic Parkinson's disease. (in Japanese) Nippon Hoigaku Zasshi 1998 / 52 (5) / 301-305. , Fonne-Pfister, R. et al, MPTP, the neurotoxin inducing Parkinson's disease, is a potent competitive inhibitor of human and rat cytochrome P450 isozymes (P450buf1, P450db1) catalyzing debrisoquine 4-hydroxylation. Biochem. Biophys. Res. Commun. 1987 / 148 (3) / 1144-1150. , Naoi, M. et al, Metabolism of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in a rat pheochromocytoma cell line, PC12h. Life Sci. 1987 / 41 (24) / 2655-2661. , Fuller, R.W. et al, Mechanisms of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) neurotoxicity to striatal dopamine neurons in mice. Prog. Neuropsychopharmacol. Biol. Psychiatry 1985 / 9 (5-6) / 687-690. , Heikkila, R.E. et al, Studies on the oxidation of the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by monoamine oxidase B. J. Neurochem. 1985 / 45 (4) / 1049-1054. , Heikkila, R.E. et al, Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine by MAO inhibitors. Nature 1984 / 311 (5985) / 467-469.
(8) Takahashi, T. et al, Cytotoxicity of endogenous isoquinolines to human dopaminergic neuroblastoma SH-SY5Y cells. J. Neural. Transm. 1997 / 104 (1) / 59-66.
(9) Wilson, J.A. et al, MPTP causes a non-reversible depression of synaptic transmission in mouse neostriatal brain slice. Brain Res. 1986 / 368 (2) / 357-360.
(10) Wu, W.R. et al, Involvement of monoamine oxidase inhibition in neuroprotective and neurorestorative effects of Ginkgo biloba extract against MPTP-induced nigrostriatal dopaminergic toxicity in C57 mice. Life Sci. 1999 / 65 (2) / 157-164. , Lee, E.H. et al, Comparitive studies of the neurotoxicity of MPTP in rats. Chin. J. Physiol. 1992 / 35 (4) / 317-336. , Hara, K. et al, Reversible serotinergic neurotoxicity of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in muose striatum studied by neurochemical and immunohistochemical approaches. Brain Res. 1987 / 410 (2) / 371-374. , Pileblad, E. et al, Catecholamine-uptake inhibitors prevents the neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mouse brain. Neuropharmacology 1985 / 24 (7) / 689-692. , Gerhardt, G. et al, Dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse : an in vivo electrochemical study. J. Pharmacol. Exp. Ther. 1985 / 235 (1) / 259-265.
(11) Deutch, A.Y. et al, 3-Acetylpyridine-induced degeneration of the nigrostriatal dopamine system : an animal model of olivopontocerebellar atrophy-associated parkinsonism. Exp. Neurol. 1989 / 105 (1) / 1-9. , Kindt, Role for monoamine oxidase-A (MAO-A) in the bioactivation and nigrostriatal dopaminergic neurotoxicity of the MPTP analog, 2'-Me-MPTP. Eur. J. Pharmacol. 1988 / 146 (2-3) / 313-318. , Heikkila, R.E. et al, Importance of monoamine oxidase in the bioactivation of neurotoxic analogs of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. Proc. Natl. Acad. Sci. U.S.A. 1988 / 85 (16) / 6172-6176. , Youngster, S.K. et al, Evaluation of the biological activity of several analogs of the dopaminergic neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. J. Neurochem. 1987 / 48 (3) / 929-934. , Sonsalla, P.K. et al, Characteristics of 1-methyl-4-(2'-methylphenyl)-1,2,3,6-tetrahydropyridine-induced neurotoxicity in the mouse. J. Pharmacol. Exp. Ther. 1987 / 242 (3) / 850-857. , Trevor, A.J. et al, Bioactivity of MPTP : reactive metabolites and possible biochemical sequelae. Life Sci. 1987 / 40 (8) / 713-719. , Youngster, S.K. et al, 1-Methyl-4-cyclohexyl-1,2,3,6-tetrahydropyridine (MCTP) : an alicyclic MPTP-like neurotoxin. Neurosci. Lett. 1987 / 79 (1-2) / 151-156. , Finnegan, K.T. et al, 1,2,3,6-tetrahydro-1-methyl-4-(methylpyrrol-2-yl)pyridine : studies on the mechanism of action of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. J. Pharmacol. Exp. Ther. 1987 / 242 (3) / 1144-1151. , Melamed, E. et al, Dopamine, but not norepinephrine or serotonine uptake inhibitors protect mice against neurotoxicity of MPTP. Eur. J. Pharmacol. 1985 / 116 (1-2) / 179-181.
(12) Matsubara, K. et al, Structural significance of azaheterocyclic amines related to Parkinson's disease for dopamine transporter. Eur. J. Pharmacol. 1998 / 348 (1) / 77-84.
(13) Gioanni, Y. et al, Nicotinic receptors in the rat prefrontal cortex ; increase in glutamate release and facilitation of mediodorsal thalamo-cortical transmission. Eur. J. Neurosci. 1999 / 11 (1) / 18-30. , Radcliffe, K.A. et al, Nicotinic modulation of glutamate and GABA synaptic transmission of hippocampal neurons. Ann. NY Acad. Sci.1999 / 868 / 591-610. , Neff, R.A. et al, Nicotine enhances presynaptic and postsynaptic glutamergic neurotransmission to activate cardiac parasympathetic neurons. Circ. Res. 1998 / 83 (12) / 1241-1247. , Ashworth, Preece, M.A. et al, Nicotinic acetylcholine receptor mediated modulation of evoked excitatory amino acid release in the nucleus tractus solitarius of the rat ; evidence from in vivo microdialysis. Brain Res. 1998 / 806 (2) / 287-291. , Aramakis, V.B. et al, Activation of muscarinic receptors modulates NMDA receptor-mediated responses in auditory cortex. Exp. Brain Res. 1997 / 113 (3) / 484-496.
(14) Matsumoto, R. R. et al, Novel NMDA/glycine site antagonists attenuate cocaine-induced convulsions. Eur. J. Pharmacol. 1997 / 338 (3) / 233-242.
(15) Hasbani, M.J. et al, Distinct roles for sodium, chloride and calcium in excitotoxic dendritic injury and recovery. Exp. Neurol. 1998 / 154 (1) / 241-258.
(16) Jensen, J.B. et al, Role of desensitization and subunit expression for kainate receptor-mediated neurotoxicity in murine neocortical cultures. J. Neurosci. Res. 1999 / 55 (2) / 208-217.
(17) Meltzer, L.T. et al, Metabotropic Glutamate receptor-mediated inhibition and excitation of substantia nigra DA neurons. Synapse 1997 / 26 (2) / 184-193.
(18) Qiu, Z.H. et al, Stimulation of NMDA receptors induces apoptosis in rat brain. Brain Res. 1996 / 725 (2) / 166-176.
(19) Holden, R.J. ,Schizophrenia, smoking and smog. Holist. Nurs. Pract. 1995 / 9 (2) / 74-82.
(20) Martinez, Z.A. et al, Effects of sustained cocaine exposure on sensori motor gating of startle in rats. Psychopharmacology (Berl.) 1999 / 142 (3) / 253-260. , Kosten ,T.A. ,Enhanced neurobehavioural effects of cocaine with chronic neurleptic exposure in rats. Schizophr. Bull. 1997 / 23 (2) / 203-213.
(21) Davis, K.L. et al, Cholinergic markers in elderly patients with early signs of Alzheimer's disease. J. Am. Med. Assoc. 1999 / 281 (15) / 1401-1406.
(22) Szekeres, P.G. et al, The relationship between agonist intrinsic activity and the rate of endocytosis of muscarinic receptors in a human neuroblastoma cell line. Mol. Pharmacol. 1998 / 53 (4) / 759-765.
(23) Gearing, M. et al, diffuse plaques in the stratium in Alzheimer disease (AD) : relationship to the striatal mosaic and selected neuropeptide markers. J. Neuropathol. Exp. Neurol. 1997 / 56 (12) / 1363-1370.
(24) Montine, T.J. et al, Central nervous system lipoptroteins in Alzheimer's disease. Am. J. Pathol. 1997 / 151 (6) / 1571-1575.
(25) Soto, J. et al, Dissociation between I2-imidazoline receptors and MAO-B activity in platelets of patients with Alzheimer's type of dementia. J. Psychiatr. Res. 1999 / 33 (3) / 251-257. , Klegeris, A. et al, Interaction of Alzheimer beta-amyloid peptide with the human monocytic cell line THP-1 results in a proteinkinase C-dependent secretion of tumor necrosis factor alpha. Brain Res. 1997 / 747 (1) / 114-121. , Saura, J. et al, Increased monoamine oxidase-B activity in plaque associated astrocytes of Alzheimer brains revealed by quantitative enzyme radioautography. Neuroscience 1994 / 62 (1) / 15-30.†
(26) Johnstone, M. et al, A central role for astrocytes in the inflammatory response to beta-amyloid : chemokines, cytokines and reactive oxygen species are produced. J. Neuroimmunol. 1999 / 93 (1-2) / 182-193.
(27) Shinotoh, H. ,PET study of cholinergic system in the brain. Rinsho Shinkeigaku 1999 / 39 (1)/ 33-35.
(28) Kryger, G. et al, structure of acetylchinesterase cmpexed with E2020 (Aricept) : implications for the design of new anti-Alzheimer drugs. Structure Fold. Des. 1999 / 7 (3) / 297-307. , Forette, F. et al, A phase 2 study in patients with Alzheimer's disease to asses the preliminary efficacy and maximum tolerated dose of rivastigmine (Exeloninfinity). Eur. J. Neurol. 1999 / 6 (4) / 423-429. , Raskind, M.A. et al, The effects of metrifonate on the cognitive ,behavioral, and functional performance of Alzheimer disease patients. Metrifonate Study Group. J. Clin. Psychiatry 1999 / 60 (5) / 318-325. , Moore, H. et al, Role of accumbens and cortical dopamine receptors in the regulation of cortical acetylcholine release. Neuroscience 1999 / 88 (3) / 811-822. , Molnar, J. et al, Effects of tricyclic compounds on membrane binding of bivalent cations, activities of AChE and some tissue proteases. In Vivo 1993 / 7 (5) / 431-434.
(29) Ohashi, Y. et al, Daily rythm of serum melatonin levels and effect of light exposure in patients with dementia of the Alzheimer's type. Biol. Psychiatry 1999 / 45 (12) / 1646-1652.
(30) Newman, S.C. ,The prevalence of depression in Alzheimer's disease and vascular dementia in a pop-sample. J. Affect. Disord. 1999 / 52 (1-3) / 169-176. , Simpson, S. et al, Neurological,correlates of depressive symptoms in Alzheimer disease and vascular dementia. J. Affect. Disord. 1999 / 53 (2) / 129-136.
(31) Heikkila, R.E. et al, Differential neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in Swiss-Webster mice from different sources. Eur. J. Pharmacol. 1985 / 117 (1) / 131-133.
(32) Alagarsamy, S. et al, Dopamine neurotoxicity in cortical neurones. Drug. alcohol. Depend. 1997 / 48 (2) / 105-111. , Nozaki, O. et al, Amines for detection of dopamine by generation of hydrogen peroxide and peroxyoxalate chemiluminescence. J. Biolumi. Chemilumin. 1996 / 11 (6) / 309-313.
(33) Morin, B. ,The protein oxidation product 3,4-dihydroxyphenylalanine (DOPA) mediates oxidative DNA damage. Biochem. J. 1998 / 330 (pt 3) / 1059-1067.
(34) Jellinger, K.A., The role of iron in neurodegeneration : prospects for pharmacotherapy of Parkinson's disease. Drugs. Aging. 1999 / 14 (2) / 115-140. , Spencer, J.P. et al, Conjugates of catecholamines with cysteine and GSH in Parkinson's disease : possible mechanisms of formation involving reactive oxygen species. J. Neurochem. 1998 / 71 (5) / 2112-2122.
(35) Snyder, R.D. et al, Enhancement of cytotoxicity and and clastogenicity of L-dopa and dopamine by manganese and copper. Mutat. Res. 1998 / 405 (1) / 1-8. , Vescovi, A. et al, Interactions of manganes with human brain glutathione-S-transferase. Toxicology 1989 / 57 (2) / 183-191.
(36) Jenner, P. et al, Oxidative stress and the pathogenesis of Parkinson's disease. Neurology 1996 / 47 (6 suppl.3) / S161-S170.
(37) Huang, C.C. et al, alteration of corticotropin releasing factor immunoreactivity in MPTP-treated rats. J. Neurosci. Res. 1995 / 41 (4) / 471-480.
(38) Matsubara, K. et al, Metabolic activation of azaheterocyclics induced dopaminergic toxicity : possible candidate neurotoxins underlying idiopathic Parkinson's disease. (japans) Nippon Hoigaku Zasshi 1998 / 52 (5) / 301-305. , Collins, M.A. et al, beta-Carboline analogues of N-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) : endogenous factors underlying idiopathic parkinsonism ? Neurosci. Lett. 1985 / 55 (2) / 179-184.
(39) Kuhn, W. et al, Plasma levels of the beta-carbolines harman and norharman in Parkinson's disease. Acta. Neurol. Scand. 1995 / 92 (6) / 451-454.
(40) Matsubara, K. et al, Metabolic activation of azaheterocyclics induced dopaminergic toxicity : possible candidateneurotoxins underlying idiopathic Parkinson's disease. (in Japanese) Nippon Hoigaku Zasshi 1998 /52 (5) / 301-305.
(41) Nagatsu, Isoquinoline neurotoxics in the brain and Parkinson's disease. Neurosci. Res. 1997 / 29 (2) / 99-111.
(42) Muller-Spahn, F. et al, Elevated response of growth hormone to graded doses of apomorphine in schizophrenic patients. J. Psychiatr. Res. 1998 / 32 (5) / 265-271. , Lee, T. et al, Am. J. Psychiatry 1980 / 137 (2) / 191-197.
(43) Dohan ,F.C. ,Genetic hypothesis of idiopathic schizophrenia : its exorphin connection. Schizophr. Bull. 1988 / 14 (4) / 489-494.
(44) Johnson, S.A. et al, Synergistic interactions between ampakines and antipsychotic drugs. J. Pharmacol. Exp. Ther. 1999 / 289 (1) / 392-397.
(45) Faustman, W.O. et al, Cerobrospinal fluid glutamate inversely correlates with positive symptom severity in unmediated male schizophrenic / schizoactive patients. Biol. Psychiatry 1999 / 45 (1) / 68-75. , Moghaddam, B. et al, Activation of glutamergic neurotransmission by ketaurine : a novel step in the pathway from NMDA receptor blockade to dopaminergic and cognitive disruptions associated with the prefrontal cortex. J. Neurosci. 1997 / 17 (8) / 2921-2927.
(46) Medvedev, A.E. et al, The influence of the antidepressant pirlindole and its dehydro-derivate on the activity of monoamine oxidase A and GABAA receptor binding. J. Neur. Transm. Suppl. 1998 / 52 / 337-42. , Auta, J. et al, Effects of negative allosteric modulators of gamma-aminobuteric acid A receptors on complex behaviuoral processes in monkeys. J. Pharmacol. Exp. Ther. 1997/280 (1) / 316-325.
(47) Deakin, J.F. et al, A two-process theory of schizophrenia : evidence from studies in post-mortem brain. J. Psychiatr. Res. 1997 / 31 (2) / 277-295.
(48) Heresco-Levy, K. et al, Efficacy of high-dose glycine in the treatment of enduring negative symptoms of schizophrenia. Arch Gen. Psychiatry 1999 / 56 (1) / 29-36.
(49) Kishimoto, H. et al, Brain imaging of affective disorders and schizofrenia. Psychiatr. Clin. Neurosci. 1998 / 52 / suppl.S212-214.
(50) Feighner, J.P. et al, Mechanism of action of antidepressant mediators. J. Clin. Psychiatry 1999 / 60 ,suppl.4 / 4-11, disc.12-3.