FK-960 [N-(4-acetyl-1-piperazinyl)-p-fluorobenzamide monohydrate], a novel putative anti-dementia drug of piperazine derivative, ameliorates memory deficits in a variety of animal models of dementia in rats and monkeys, and also augments long-term potentiation (LTP) in the mossy fiber-CA3 pathway in guinea-pig hippocampal slices. FK-960 acts as Serotonin modulator. FK-960 had been in phase II clinical trials by Fujisawa Pharmaceutical (now Astellas) for the treatment of Alzheimer's disease (AD). However this study was suspended. In 2003 Phase-II for Alzheimer's disease in USA was discontinued and in Jul 2004 - Phase-II for Cognition disorders in Europe.

PHA-543613 was discovered by Pfizer and has been under development primarily as a potential treatment of schizophrenia. PHA-543613 acts as an agonist to the Neuronal acetylcholine receptor protein alpha-7 subunit. A single human trial was conducted in healthy human volunteers, but the compound has been studied extensively in rat models for schizophrenia as well as Parkinson's disease and Alzheimer's disease.

Tacrine is a parasympathomimetic- a reversible cholinesterase inhibitor that is indicated for the treatment of mild to moderate dementia of the Alzheimer's type. An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of cholinergic neurons in the cerebral cortex, nucleus basalis, and hippocampus. Tacrine is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine at cholinergic synapses through reversible inhibition of its hydrolysis by acetylcholinesterase. If this proposed mechanism of action is correct, tacrine's effect may lessen as the disease progresses and fewer cholinergic neurons remain functionally intact. There is no evidence that tacrine alters the course of the underlying dementing process. The mechanism of tacrine is not fully known, but it is suggested that the drug is an anticholinesterase agent which reversibly binds with and inactivates cholinesterases. This inhibits the hydrolysis of acetylcholine released from functioning cholinergic neurons, thus leading to an accumulation of acetylcholine at cholinergic synapses. The result is a prolonged effect of acetylcholine. is used for the palliative treatment of mild to moderate dementia of the Alzheimer's type. Tacrine was marketed under the trade name Cognex. Because of its liver toxicity and attendant requirement for monitoring liver function, tacrine prescriptions dropped after other acetylcholinesterase inhibitors were introduced, and its use has been largely discontinued.

Tacrine is a parasympathomimetic- a reversible cholinesterase inhibitor that is indicated for the treatment of mild to moderate dementia of the Alzheimer's type. An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of cholinergic neurons in the cerebral cortex, nucleus basalis, and hippocampus. Tacrine is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine at cholinergic synapses through reversible inhibition of its hydrolysis by acetylcholinesterase. If this proposed mechanism of action is correct, tacrine's effect may lessen as the disease progresses and fewer cholinergic neurons remain functionally intact. There is no evidence that tacrine alters the course of the underlying dementing process. The mechanism of tacrine is not fully known, but it is suggested that the drug is an anticholinesterase agent which reversibly binds with and inactivates cholinesterases. This inhibits the hydrolysis of acetylcholine released from functioning cholinergic neurons, thus leading to an accumulation of acetylcholine at cholinergic synapses. The result is a prolonged effect of acetylcholine. is used for the palliative treatment of mild to moderate dementia of the Alzheimer's type. Tacrine was marketed under the trade name Cognex. Because of its liver toxicity and attendant requirement for monitoring liver function, tacrine prescriptions dropped after other acetylcholinesterase inhibitors were introduced, and its use has been largely discontinued.

Dihydroergocornine is an ergot alkaloid, one of the three components of ergoloid (trade name Hydergine). Dihydroergocornine (as the component of Ergoloid mesylates) has been used to treat dementia and age-related cognitive impairment (such as in Alzheimer disease), as well as to aid in recovery after stroke. There is no specific evidence which clearly establishes the mechanism by which Hydergine® (ergoloid mesylates) preparations produce mental effects, nor is there conclusive evidence that the drug particularly affects cerebral arteriosclerosis or cerebrovascular insufficiency. Hydergine may stimulates dopaminergic and serotonergic receptors and blocks alpha-adrenoreceptors.

Gallic acid is a polyphenol found in a variety of foods and herbs. Several studies have shown thta gallic acid has neuroprotective and anti-oxidant properties and can be a promising candidate for the treatment of cancer, cardiovascular diseases, neurodegenerative disorders, fatty liver disease and many others. Gallic acid acts by protecting cells against oxidative damage caused by reactive species often encountered in biological systems including, hydroxyl, superoxide and peroxyl and the non-radicals, hydrogen peroxide and hypochlorous acid. However, its ability to induce apoptosis, is mainly associated with its prooxidant, rather than antioxidant behavior.

Gallic acid is a polyphenol found in a variety of foods and herbs. Several studies have shown thta gallic acid has neuroprotective and anti-oxidant properties and can be a promising candidate for the treatment of cancer, cardiovascular diseases, neurodegenerative disorders, fatty liver disease and many others. Gallic acid acts by protecting cells against oxidative damage caused by reactive species often encountered in biological systems including, hydroxyl, superoxide and peroxyl and the non-radicals, hydrogen peroxide and hypochlorous acid. However, its ability to induce apoptosis, is mainly associated with its prooxidant, rather than antioxidant behavior.

Fursultiamine, also known as thiamine tetrahydrofurfuryl disulfide (TTFD) is an oral FDA- approved thiamine derivative for treating vitamin B1 deficiency and is very rapidly metabolized into thiamine. Fursultiamine possesses a mild beneficial effect in patients with Alzheimer's disease. The improvement could be observed not only in their emotional or other mental symptoms but also in intellectual function. Only mildly impaired subjects showed cognitive improvement. In addition was shown, that fursultiamine have a beneficial clinical effect on some autistic children. Some relatively recent experiments have revealed that fursultiamine was a unique antagonist of hepcidin in vitro that could serve as a template for the development of drug candidates that inhibit the hepcidin-ferroportin interaction. This inhibition is a key for the treatment of anemia of inflammation (AI), a common in patients with infection, autoimmune diseases, cancer, and chronic kidney disease.

L-acetylcarnitine or acet-L-carnitine, a compound, naturally produced by the body, is necessary for fatty-acid metabolism and energy production. It is often taken as a dietary supplement. The mechanisms of action of acetylcarnitine have not been fully elucidated, but it seems that the main role of acetylcarnitine is to donate an acetyl group during fatty acid metabolism to help transport fatty acids, such as acetyl CoA, into the mitochondrial matrix where fatty acid metabolism occurs. L-acetylcarnitine is an investigational drug, which is approved in some countries, for example in Italy for diabetic neuropathy. Phase IV of clinical trials have revealed, that it also effective agent to treat the Alzheimer's disease. In contrary, the efficacy of L-acetylcarnitine as a prophylaxis in migraine patients did not provide evidence of benefit for efficacy. Besides, Acetyl-L-carnitine was in clinical trial Phase III to investigate its efficacy in the treatment of peripheral sensory neuropathy that anti-cancer chemotherapeutics induce. Recently published article unexpectedly discovered that this drug increased chemotherapy-induced peripheral neuropathy in a randomized trial.

Methylinositol is a natural product in the family of inositols. It is found in many foods as well as pine tree bark. Methylinositol is found naturally in many foods and is commercially available as an approved food supplement. Methylinositol can mediate insulin action to improve glycemic control and insulin sensitivity in patients with type 2 diabetes mellitus, especially in patients with insulin resistance. It plays a positive role in regulating insulin-mediated glucose uptake in the liver through translocation and activation of the PI3K/Akt signaling pathway. The compound also modulates gamma-secretase to reduce A-betta production while sparing cleavage of the gamma-secretase substrate Notch. Methylinositol improves cognitive function and memory deficits in preclinical models of Alzheimer's disease (AD) neuropathology. Methylinositol was will tolerated in the population of AD subjects of varying age and severity. No serious adverse effects were detected in clinical trials. Many plant-derived compounds have excellent therapeutic potential against various human ailments. It was shown, that methylinositol mitigates tumor growth by modulating interleukins and hormones and induces apoptosis in rat breast carcinogenesis through inhibition of NF-κB.