Effects of Centrophenoxine on the Monovalent Electrolyte Contents of the Large Brain Cortical Cells of Old Rats

Zs.‐Nagy, Imre; Pieri, Carlo; Giuli, C.; Moro, M. Del

doi:10.1159/000212326

Cited by 38 publications

(2 citation statements)

References 19 publications

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“…However, post treatment with CpH resulted in a significant improvement in the cognitive behavior of animals as they escaped only 3.2 trials as compared to Al exposed animals. Zs-Nagy et al [21] also reported that CpH supplementation produced marked improvement in learning, memory, and mental alertness. Similarly, Nandy [22] reported a significant improvement of symptoms such as fatigue, irritability, confusional states, and loss of memory in the geriatric patient treated with CpH.…”

Section: Discussionmentioning

confidence: 95%

Biochemical alterations in rat brain following aluminum exposure: Protection with centrophenoxine

Nehru

Bhalla

2007

Toxicological & Environmental Chemistry

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Aluminum (Al) is a neurotoxicant potentially affecting ionic, cholinergic, and dopaminergic neurotransmission in the central nervous system. These alterations are known to be associated with learning ability, adaptive responses, and other aspects of behavior. The present experiment was designed to study the neurotoxic consequences of Al exposure on neurotransmitters like dopamine (DA), serotonin (5-HT), norepinephrine (NE) along with the activity of acetylcholinesterase (AChE). Furthermore, Centrophenoxine (CpH) was administered as a post treatment to evaluate its potential in Al-induced neurotoxicity. The cognitive functions and memory loss were also studied after both Al and CpH administration. Al was administered orally at a dose of 40 mg kg À1 day À1 for a period of 8 weeks, whereas CpH was administered intraperitoneally at a dose of 100 À1 mg kg À1 day À1 for a period of 6 weeks. The study was carried out in four regions of the brain, namely cerebrum, cerebellum, medulla oblongata, and hypothalamus. A significant reduction in AChE activity and different neurotransmitters was observed after Al exposure in the regions. CpH as a post treatment proved beneficial in restoring these alterations. Al exposure also affected the cognitive functions and short-term memory, which were significantly improved following CpH post treatment.

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Section: Discussionmentioning

confidence: 95%

Biochemical alterations in rat brain following aluminum exposure: Protection with centrophenoxine

Nehru

Bhalla

2007

Toxicological & Environmental Chemistry

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“…As explained by the MHA, the age‐dependent decline of the passive potassium permeability in the nerve cells is a key issue in brain aging. CPH treatment for 60 days (80‐100 mg/kg) in old rats reincreased the passive potassium permeability of the neuronal‐cell membrane, that is, it decreased the intracellular potassium content and rehydrated the cytoplasm of brain neurons significantly 62,63. BCE‐001 had the same effect, though a lower dose (60 mg/kg) and a shorter period (3‐4 weeks) of treatment were sufficient to reach the same level as these improvements in rats (unpublished observations).…”

Section: In Vivo Biological Effects Of Cph and Bce‐001mentioning

confidence: 99%

Pharmacological Interventions against Aging through the Cell Plasma Membrane

Zs.‐Nagy

2002

Annals of the New York Academy of Sciences

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As was shown in a recent review by this author (Ann. N.Y. Acad. Sci., 928: 187-199, 2001), oxyradicals cannot be considered only as harmful by-products of the oxidative metabolism, but living cells and organisms implicitly require their production. This idea is supported by numerous facts and arguments, the most important of which is that the complete inhibition of the oxyradical production by KCN (or by any block of respiration) kills the living organisms long before the energy reserves would be exhausted. This new theoretical approach not only helps our understanding of the normal functions of the living organisms, such as the basic memory mechanisms in the brain cells, but also helps in identifying the site-specific, radical-induced damaging mechanisms that represent the undesirable side effects of oxygen free radicals. First of all, these effects make the cell plasma membrane vulnerable and cause a series of intracellular functional disorders, as described by the membrane hypothesis of aging (MHA). The logical way for any antiaging intervention therefore should be to increase the available number of loosely bound electrons inside the plasma membrane that are easily accessible for OH(*) free radical scavenging. The present review summarizes the available knowledge regarding the theory of the use of membrane-related antiaging pharmaca, like centrophenoxine (CPH), tested in both animal experiments and human clinical trials. A modified, developed version of CPH coded as BCE-001 is also reported.

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Drug treatments for cognitive impairment due to ageing and disease: Current and future strategies

Dowson

1989

Int J Geriat Psychiatry

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SUMMARYAs the pathological changes in Alzheimer dementia include degeneration of cholinergic neurones, several strategies have been used to enhance the activity of remaining cholinergic neurones, including the administration of anticholinesterases. Other drugs which have been claimed to have a beneficial effect on cognitive impairment in the aged and in various diseases include dihydroergotoxine (the most widely used in clinical practice), bufluomedil, piracetam and centrophenoxine. These drugs, and the many other compounds which have been investigated, have a wide variety of actions. However, drugs which improve the function of neuronal populations affected by pathogenic mechanisms can only be palliative. Future strategies for drug treatments will be directed towards reducing the adverse effects of the ageing process (which may include an increased susceptibility to a range of diseases) and neutralizing the pat'hogenic mechanisms related to genetic factors, infections, toxins, trauma, anoxia and diet. One mechanism which may operate in ageing and in some pathological changes is the production of 'free radicals', which can cause cellular damage. Prophylactic administration of drugs with antioxidant activity can reduce adverse effects of this process in animal models, and such treatments may also protect the brain from the effects of anoxia and other pathogenic mechanisms. Other drugs with therapeutic potential include antagonists of the excitatory effects of glutamate and aspartate.

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Effects of Centrophenoxine on the Monovalent Electrolyte Contents of the Large Brain Cortical Cells of Old Rats

Cited by 38 publications

References 19 publications

Biochemical alterations in rat brain following aluminum exposure: Protection with centrophenoxine

Biochemical alterations in rat brain following aluminum exposure: Protection with centrophenoxine

Pharmacological Interventions against Aging through the Cell Plasma Membrane

Drug treatments for cognitive impairment due to ageing and disease: Current and future strategies

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