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.

Cyclandelate is a vasodilator developed for the treatment of cardiovascular diseases. The drug was used in many countries for such diseases as intermittent claudication, arteriosclerosis obliterans, thrombophlebitis, nocturnal leg cramps, local frostbite, Raynaud's phenomenon. In the USA it was also approved for intermittent claudication and cognitive dysfunction in Alzheimer's disease under the name Cyclospasmol. Cyclandelate exerts its effect by blocking calcium channels and inhibiting smooth muscles contration. Cyclandelate was withdrawn from the market in the USA for lack of effectiveness.

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.

Vanillin (4-hydroxy-3-methoxybenzaldehyde), a pleasant smelling organic aromatic compound, is widely used as a flavoring additive in food, beverage, cosmetic and drug industries. It is reported to cross the blood brain barrier and also displayed antioxidant and neuroprotective activities. Vanillin is a natural substance widely found in many plant species and often used in beverages, foods, cosmetics, and pharmaceutical products. Antioxidant and anticancer potential have been described for this compound. Vanillin has been classified as a bioantimutagen and is able to inhibit mutagenesis induced by chemical and physical mutagens in various cell systems. Vanillin, a selective agonist of TRPV1, has been shown to attenuate i.c.v. STZ and AlCl3+d-galactose induced experimental Alzheime's disease (AD).

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.

Ginkgolide B belongs to the class of organic compounds known as ginkgolides and bilobalides. These are diterpene lactones with a structure based either on the gingkolide or the bilobalide skeleton. The ginkgolide skeleton is a very rigid structure consisting of hexacyclic C20 trilactone. The cis-fused F/A/D/C ring junction forms an empty semi-ball hole, the D ring contains a cage form tetrahydrofuran ring which occupies the center of the empty hole, and the oxygen atoms of the D,C and F ring and 10-hydroxyl group consist of an analogous crown ether structure. Ginkgolide B is one of the ginkgolides isolated from the leaves of the Ginkgo biloba tree. The Ginkgolide B is the most potent antagonist of platelet activating factor (PAF) and exhibits therapeutic action in a variety of diseases mainly by the PAF receptor. The ginkgolide B possesses a number of beneficial effects such as anti-inflammatory, anti-allergic, antioxidant, and neuroprotective effects. It promotes the proliferation, migration and adhesion of endothelial progenitor cells, and the induction of angiogenesis through vascular endothelial factor (VEGF). Ginkgolide B is considered a valid non-pharmacological (or nutraceutical) approach to the prophylaxis of both migraine with and without aura. Effects of ginkgolide B include reduction of Ca2+-stimulated intracellular events, scavenging of free radicals, modulation of central nervous system glutamatergic transmission and reduction of antiplatelet activating factor (PAF) levels in brain. Ginkgolide B is an active component of EGb, a standardised extract of Ginkgo biloba leaves. Ginkgolide B is one of the major components of EGb-761.

Smilagenin (also known as PYM50028 and Cogane) is a constituent of Jamaican sarsaparilla (Smilax ornata) and is a neuroprotectant that has been evaluated in Phase II clinical trials in Parkinson's disease and Alzheimer's disease. On 27 September 2011, the European Commission to Phytopharm plc, United Kingdom, granted orphan designation for smilagenin for the treatment of amyotrophic lateral sclerosis. The details of the mechanism of action of smilagenin are incomplete but involve the upregulation of neurotrophic factors including Glial cell line-derived neurotrophic factor and brain-derived neurotrophic factor.

Honokiol is a biphenolic natural product isolated from the bark and leaves of Magnolia plant spp. Honokiol possesses anti-carcinogenic, anti-inflammatory, anti-oxidative, anti-angiogenic as well as the inhibitory effect on malignant transformation of papillomas to carcinomas in vitro and in vivo animal models without any appreciable toxicity. Honokiol affects multiple signaling pathways, molecular and cellular targets including nuclear factor-κB (NF-κB), STAT3, epidermal growth factor receptor (EGFR), cell survival signaling, cell cycle, cyclooxygenase and other inflammatory mediators, etc. Honokiol can permeate the blood-brain barrier and the blood-cerebrospinal fluid to increase its bioavailability in neurological tissues. Diverse studies have provided evidence on the neuroprotective effect of honokiol in the central nervous system, due to its potent antioxidant activity, and amelioration of the excitotoxicity mainly related to the blockade of glutamate receptors and reduction in neuroinflammation. Honokiol can attenuate neurotoxicity exerted by abnormally aggregated Abeta in Alzheimer's disease. Honokiol is being developed by Huons as HL tablet for the treatment of alcoholic and non-alcoholic fatty liver.

Fulvic acid is primarily studied for its effects on plants and soil. Fulvic acid is an organic and natural electrolyte. Depending on the situation, Fulvic acid can act as an electron donor or acceptor and an oxidizer or reducer. Fulvic acid has exhibited the ability to enhance the availability and adsorption of nutrients as well as prolong their time of residence. In the chick animal model Fulvic acid disturbed the processing of procollagen II in articular cartilage. Fulvic acid has being shown to attenuate homocysteine-induced cyclooxygenase-2 expression in human monocytes. Fulvic acid, the main active principle of Shilajit (a natural substance found mainly in the Himalayas), blocks tau self-aggregation, opening an avenue toward the study of Alzheimer's therapy. People take fulvic acid by mouth for brain disorders such as Alzheimer’s disease, as well as respiratory tract infections, cancer, fatigue, heavy metal toxicity, and preventing a condition in which the body tissues do not receive enough oxygen (hypoxia).

Wogonin is an O-methylated flavone compound isolated from Scutellaria baicalensis. Wogonin is an a positive allosteric modulator of benzodiazepine site of the GABAA ion channel, and displays anxiolytic properties in animal models. It possesses anti-tumor effect in models of osteosarcoma and lung cancer. Hepatoprotective action of wogonin was demonstrated in the mouse model of alcoholic liver disease and in a model of nonalcoholic fatty liver disease, where it was shown that wogonin upregulates PPAR-gamma and PPARalpha respectively. Wogonin possess chondroprotective action which was demonstrated in models of osteoarthritis.