Herbal medicines vs modern medicine,male yeast infection confused with herpes,energy saving electric 400w panel heater,herpes dating site indianapolis jobs - 2016 Feature

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Even from the scanty evidence in the scriptural texts still left for posterity, it is easy to infer that valuable information about the advancement of science and technology in ancient days has been lost. The arrows which got stuck to the body had to be removed carefully and gushing of blood stopped. The Brahmastra aimed by Indrajit immobilised the entire monkey legion and also Sri Rama and Lakshmana but the medicines brought by Hanuman worked wonders and all of them were ready again to attack the Ravana warriors. Because herbal medicines are made from all-natural ingredients, they are much safer than lab-made drugs.
Although there are cases wherein patients developed bad reaction from a certain herbal medicine, this is often caused by contamination.
There are cases wherein doctors wrongfully prescribed herbal drugs and this can cause slight discomforts and side effects too. Did you know that most synthetic drugs available on the market are just replicas of herbal medication?
In nature, herbs contain a combination of medicinal properties that are arranged harmoniously. Here’s how the whole pharmaceutical industry work: a drug company will isolate a certain molecule from a medicinal herb and gets a patent for it. Science, Technology and Medicine open access publisher.Publish, read and share novel research. Traditional and Modern Medicine Harmonizing the Two Approaches in the Treatment of Neurodegeneration (Alzheimer’s Disease – AD)Bowirrat Abdalla, Mustafa Yassin, Menachem Abir, Bishara Bisharat and Zaher Armaly[1] EMMS Nazareth-The Nazareth Hospital, Nazareth1. There were immediate cures for gashes and grievous injury as also treatment for fractures and dislocations. The combat also proved the futility of human beinga€™s endeavour to subvert the arrangements made by God. Ravana least expected that the monkeys could face leaders on his side like Kumbakarna and Indrajit. Subramania Somayajulu said that no one who followed the path of Righteousness would be let down by the Supreme Being.
For instance, garlic’s powerful antiviral, antibacterial, antifungal and anti-inflammatory compounds work just as well as any non-steroidal anti-inflammatory drugs or NSAIDs! Studies show that manufactured items – including synthetic drugs – are not superior or effective than natural items, such as herbal meds.
As long as you take high-quality herbal meds from a reputable company, you can expect less of the usual side-effects associated with synthetic medication. That’s right, most drugs found in your local pharmacy are synthesized to isolate a herb’s active ingredient, eliminating other compounds found in the medicinal plant. Because the innovation is exclusive to said company, the patent could be worth billions of dollars. Not because synthetic drugs are more effective but because consumers are paying for the so-called “innovations” developed by the drug company in synthesizing the active compounds of its main ingredients.
IntroductionNeurodegenerative disorders, Primarily, are multifactorial diseases characterized by chronic and progressive loss of neurons in discrete areas of the brain, causing debilitating symptoms and globally decreasingcognitivefunction such as dementia, loss of memory, loss of sensory or motor capability, decreased overall quality of life and well-being, disability, and eventually, premature death. Occasions demanded, particularly during wars, that wounded soldiers should be attended to and sent to field service back within a few hours to overcome manpower shortage. People who fell unconscious were brought back to normalcy by making them inhale a special type of herb.
As his plans failed and death stared at him he was reminded about the curse incurred by him for his misconduct.
This was proved by Lakshmana who released an arrow, swearing in the name of lord Rama that should He really be the replica of Dharma, the foe should be vanquished. Herbal medications are better in quality because their medicinal compounds stay uniform and harmonious. Imagine how much money drug companies make by isolating the active ingredients of herbal plants. For most neurodegenerative diseases, there is little or no treatment; at best, treatments are symptomatic in nature and do not prevent or slow the progression of disease. The battle between Sri Rama and Ravana in the Ramayana gives scope to reflect on the genius of our forbears and the efficacy of Ayurveda.
In today’s post, we are listing down reasons why herbal medicine is superior to synthetic drugs. Herbal plants may contain various compounds that look chaotic, but there is a natural order within these compounds.
Herbal medicine may be less expensive than most synthetic drugs, but this does not mean they are less effective in treating certain diseases. Clearly, an understanding of pathological progression can help to identify points of intervention and lead to promising therapeutic approaches. On the other hand, store-bought drugs are like a patchwork of synthetic and natural compounds that may harm the body. A fundamental approach for reducing the burden of neurodegenerative diseases is thus to slow or halt progression, and ultimately, to prevent the onset of the disease process.
Strategies for neurorescue, neurorepair, neuroprotection or treatment are being actively pursued by the basic, translational, and clinical research communities. As our population ages, the already enormous impact of neurodegeneration on society will become even larger without better prevention and treatment. The death or malfunction of these nerve cells, called neurons, causes changes in one’s memory, behavior and Ability to think clearly. In Alzheimer’s disease (AD), these brain changes eventually impair an individual’s Ability to carry out such basic bodily functions as walking and swallowing. As aged population dramatically increases in these decades, efforts should be made on the intervention for curing age-associated neurodegenerative diseases such as AD.
In the United States in 2011, the cost of health care, long-term care, and hospice services for people aged 65 years and older with AD and other dementias was expected to be $183 billion, and this figure does not include the contributions of unpaid caregivers(3).
Currently, an autopsy or brain biopsy is the only way to make a definitive diagnosis of AD. In clinical practice, the diagnosis is usually made on the basis of the history and findings on Mental Status Examination.Symptomatic therapies are the only treatments available for AD. The standard medical treatments include cholinesterase inhibitors and a partial N -methyl-D-aspartate (NMDA) antagonist. Psychotropic medications are often used to treat secondary symptoms of AD, such as depression, agitation, and sleep disorders.
Historical backgroundIn 1901, a German psychiatrist named Alois Alzheimer observed a patient at the Frankfurt Asylum named Mrs. This 51-year-old woman suffered from a loss of short-term memory, among other behavioral symptoms that puzzled Dr. Alzheimer sent her brain and her medical records to Munich, where he was working in the lab of Dr. By staining sections of her brain in the laboratory, he was able to identify amyloid plaques and neurofibrillary tangles (4).A speech given by Dr. Alzheimer on November 3, 1906, was the first time the pathology and the clinical symptoms of the disorder, which at the time was termed presenile dementia, were presented together.
In the past 15-20 years, dramatic progress has been made in understanding the neurogenetics and pathophysiology of AD. Four different genes have been definitively associated with AD, and others that have a probable role have been identified. The mechanisms by which altered amyloid and tau protein metabolism, inflammation, oxidative stress, and hormonal changes may produce neuronal degeneration in AD are being elucidated, and rational pharmacologic interventions based on these discoveries are being developed.Rapid progress towards understanding the molecular underpinnings of neurodegenerative disorders such as AD is revolutionizing drug discovery for these conditions. Furthermore, the development of models for these disorders is accelerating efforts to translate insights related to neurodegenerative mechanisms into disease-modifying therapies.AD or Alzheimer's-type dementia is a progressive degeneration of brain tissue that primarily strikes people over age 65. Attention tends to stray, simple calculations become impossible, and ordinary daily activities grow increasingly difficult, accompanied by bewilderment and frustration.
AD characterized clinically by progressive memory deficits, impaired cognitive function, and altered and inappropriate behavior. Aging represents the most important risk factor and dementia has become one of the major challenges in our societies due to the universal phenomenon of population aging in the world. Brain regions involved in learning and memory processes, including the temporal and frontal lobes as well as the hippocampus, are reduced in size in AD patients as the result of degeneration of synapses and death of neurons.
AD is considered as a protein aggregation disorder, based on two key neuropathological hallmarks, namely the hyperphosphorylation of the tau protein resulting in the formation of neurofibrillary tangles (NFTs), and the increased formation and aggregation of amyloid-beta peptide (A?) derived from amyloid precursor protein (APP) (6). Although the exact underlying cause initiating the onset of AD is still unclear, an imbalance in oxidative and nitrosative stress, intimately linked to mitochondrial dysfunction, characterizes already early stages of AD pathology.3. Etiology of Alzheimer’s Disease (AD)The cause of AD is not entirely known, but is thought to include both genetic and environmental factors (Multifactorial). A diagnosis of AD is made when certain symptoms are present, and by making sure other causes of dementia are not present (DSM-IV criteria).The only way to know for certain that someone has AD is to examine a sample of their brain tissue after death.
As a result, areas of the brain that normally work together become disconnected.Healthy neurons have an internal support structure partly made up of structures called microtubules. These microtubules act like tracks, guiding nutrients and molecules from the body of the cell down to the ends of the axon and back. A special kind of protein, tau, binds to the microtubules and stabilizes them.In AD, tau is changed chemically. When this happens, the microtubules disintegrate, collapsing the neuron’s transport system (see the image below). Certain nerve cells in the brain stop working, lose connections with other nerve cells, and finally die. The destruction and death of these nerve cells causes the memory failure, personality changes, problems in carrying out daily activities, and other features of the disease.The accumulation of SPs primarily precedes the clinical onset of AD. NFTs, loss of neurons, and loss of synapses accompany the progression of cognitive decline(8).Considerable attention has been devoted to elucidating the composition of SPs and NFTs to find clues about the molecular pathogenesis and biochemistry of AD.
In AD, hyperphosphorylated tau accumulates in the perikarya of large and medium pyramidal neurons. Somewhat surprisingly, mutations of the tau gene result not in AD but in some familial cases of frontotemporal dementia.Since the time of Alois Alzheimer, SPs have been known to include a starchlike (or amyloid) substance, usually in the center of these lesions.
The amyloid substance is surrounded by a halo or layer of degenerating (dystrophic) neurites and reactive glia (both astrocytes and microglia).One of the most important advances in recent decades has been the chemical characterization of this amyloid protein, the sequencing of its amino acid chain, and the cloning of the gene encoding its precursor protein (on chromosome 21).
These advances have provided a wealth of information about the mechanisms underlying amyloid deposition in the brain, including information about the familial forms of AD. Although the amyloid cascade hypothesis has gathered the most research financing, other interesting hypotheses have been proposed. Among these are the mitochondrial cascade hypotheses(10).In addition to NFTs and SPs, many other lesions of AD have been recognized since Alzheimer’s original papers were published. Neurofibriliary tangles and senile plaques Plaques are dense, mostly insoluble deposits of protein and cellular material outside and around the neurons. Plaques are made of beta-amyloid (A?), a protein fragment snipped from a larger protein called amyloid precursor protein (APP).

Plaques may begin to develop as early as the fifth decade of life(12).Whether A? plaques themselves cause AD or whether they are a by-product of the AD process is still unknown. It is known that changes in APP structure can cause a rare, inherited form of AD.Tangles are insoluble twisted fibers that build up inside the nerve cell. Although many older people develop some plaques and tangles, the brains of people with AD have them to a greater extent, especially in certain regions of the brain that are important in memory. As AD progresses, NFTs accumulate in many other cortical regions, beginning in high-order association regions and less frequently in the primary motor and sensory regions.SPs also accumulate primarily in association cortices and in the hippocampus.
Plaques and tangles have relatively discrete and stereotypical patterns of laminar distribution in the cerebral cortex, which indicate predominant involvement of corticocortical connections.Although NFTs and SPs are characteristic of AD, they are not pathognomonic. NFTs are found in several other neurodegenerative disorders, includingprogressive supranuclear palsyand dementia pugilistica (chronic traumatic encephalopathy).
SPs may occur in normal aging.Therefore, the mere presence of these lesions is not sufficient to support the diagnosis of AD.
These lesions must be present in sufficient numbers and in a characteristic topographic distribution to fulfill the current histopathologic criteria for AD. There is consensus that the presence of even low numbers of NFTs in the cerebral neocortex with concomitant SPs is characteristic of AD.Some authorities believed that NFTs, when present in low densities and essentially confined to the hippocampus, were part of normal aging. Amyloid hypothesis versus tau hypothesisA central but controversial issue in the pathogenesis of AD is the relationship between amyloid deposition and NFT formation. At high concentrations, the fibrillar form of A? has been shown to be neurotoxic to cultured neurons.Cultured cortical and hippocampal neurons treated with A? protein exhibit changes characteristic of apoptosis (self-regulated cell destruction), including nuclear chromatin condensation, plasma membrane blebbing, and internucleosomal DNA fragmentation.
The fibrillar form of A? has also been shown to alter the phosphorylation state of tau protein.The identification of several point mutations within theAPPgene in some patients with early-onset familial AD and the development of transgenic mice exhibiting cognitive changes and SPs also incriminate A? in AD.
The apolipoprotein E (APOE) E4 allele, which has been linked with significantly increased risk for developing AD, may promote inability to suppress production of amyloid, increased production of amyloid, or impaired clearance of amyloid with collection outside of the neuron.Autopsies have shown that patients with 1 or 2 copies of the APOE E4 allele tend to have more amyloid. Additional evidence comes from recent experimental data supporting the role of presenilins in A? metabolism, as well as findings of abnormal production of A? protein in presenilin-mutation familial AD.Although very popular, the amyloid hypothesis is not uniformly accepted. On post-mortem analysis, amyloid plaques may be undetectable in the brains of patients who had severe AD but may be present in the brains of elderly patients who did not have dementia(13).Dementia severity correlates better with the number of neocortical NFTs than with SPs. Destabilization of the microtubular system is speculated to disrupt the Golgi apparatus, in turn inducing abnormal protein processing and increasing production of A?. Granulovacuolar degeneration and neuropil threats Granulovacuolar degeneration occurs almost exclusively in the hippocampus. Neuropil threads are an array of dystrophic neurites diffusely distributed in the cortical neuropil, more or less independently of plaques and tangles. Cholinergic neurotransmission and Alzheimer diseaseThe cholinergic system is involved in memory function, and cholinergic deficiency has been implicated in the cognitive decline and behavioral changes of AD.
Activity of the synthetic enzyme choline acetyltransferase (CAT) and the catabolic enzyme acetylcholinesterase are significantly reduced in the cerebral cortex, hippocampus, and amygdala in patients with AD.The nucleus basalis of Meynert and diagonal band of Broca provide the main cholinergic input to the hippocampus, amygdala, and neocortex, which are lost in patients with AD. Loss of cortical CAT and decline in acetylcholine synthesis in biopsy specimens have been found to correlate with cognitive impairment and reaction-time performance. Studies have demonstrated that an increase in oxidative damage selectively occurs within the brain regions involved in regulating cognitive performance(14).Oxidative damage potentially serves as an early event that then initiates the development of cognitive disturbances and pathological features observed in AD. A decline in protein synthesis capabilities occurs in the same brain regions that exhibit increased levels of oxidative damage in patients with mild cognitive impairment (MCI) and AD. Protein synthesis may be one of the earliest cellular processes disrupted by oxidative damage in AD(15).Oxidative stress is believed to be a critical factor in normal aging and in neurodegenerative diseases such asParkinson disease,amyotrophic lateral sclerosis, and AD. The apoptotic pattern of cellular death seen in oxidative stress is similar to that produced by A? peptide exposure, and A? neurotoxicity is attenuated by antioxidants such as vitamin E. Genetics causesAlthough most cases of AD are sporadic (ie, not inherited), familial forms of AD do exist.
Autosomal dominant AD, which accounts for less than 5% of cases, is almost exclusively early onset AD; cases occur in at least 3 individuals in 2 or more generations, with 2 of the individuals being first-degree relatives(25). Familial clustering represents approximately 15–25% of late-onset AD cases and most often involves late-onset AD. Nonetheless, the mutations that have been found to date account for less than half of all cases of early-onset AD.Other than the apolipoprotein E epsilon 4 (APOE E4) genotype, no polymorphisms in other genes have been consistently found to be associated with late-onset AD. However, genome-wide association studies have identified the following additional susceptibility loci(26).6.
APPmutationsThe observation that patients with Down syndrome (trisomy 21) develop cognitive deterioration and typical pathological features of AD by middle age led to the discovery of the APP gene on chromosome 21. Simultaneously, a locus segregating with a minority of early-onset familial AD kindreds was mapped to this chromosome, in the same region as the APP gene.
Subsequently, several missense mutations within the APP gene that resulted in amino acid substitutions in APP were identified in these familial AD kindreds. PS1and PS2 mutationsApproximately 50-70% of early-onset autosomal-dominant AD cases appear to be associated with a locus (AD3) mapped by genetic linkage to the long arm of chromosome 14 (14q24.3). Numerous missense mutations have been identified on a strong candidate gene, called PS1.At the same time, another autosomal dominant locus responsible for early-onset AD was localized to chromosome 1. APOEThe gene encoding the cholesterol-carrying apolipoprotein E (APOE) on chromosome 19 has been linked to increased risk for AD, principally late-onset but also some early-onset cases. The APOE E2 allele, the least prevalent of the 3 common APOE alleles, is associated with the lowest risk of developing AD(27),with a lower rate of annual hippocampal atrophy and higher cerebrospinal fluid A? and lower phosphotau, suggesting less AD pathology (28).
The E3 allele confers intermediate risk of developing AD, with less risk than the E4 allele. A collaborative study has suggested that APOE E4 exerts its maximal effect before the age of 70 years.Many APOE E4 carriers do not develop AD, and many patients with AD do not have this allele. Therefore, the presence of an APOE E4 allele does not secure the diagnosis of AD, but instead, the APOE E4 allele acts as a biological risk factor for the disease, especially in those younger than 70 years.8. Treatment of Alzheimer's disease – From medical chemistry to plantsThe worldwide population and especially the wesearn and U.S. Within the next 50 years, the incidence of Alzheimer'sis expected to quadruple, affecting one in 45 Americans.Today, there is still no cure for Alzheimer's.
People with the disease progressively lose memory and the ability to function as Alzheimer's advances.Several different types of medications are used to treat the memory loss, behavior changes, sleep problems, and other symptoms of AD.
These medications won't stop the disease, but they can slow down the symptoms for a few months or even years. Cholinesterase inhibitionNumerous lines of evidence suggest that cholinergic systems that modulate information processing in the hippocampus and neocortex are impaired early in the course of AD.
These observations have suggested that some of the clinical manifestations of AD are due to loss of cholinergic innervation to the cerebral cortex.Centrally acting ChEIs prevent the breakdown of acetylcholine.
Since the other ChEIs have become available, tacrine has rarely been prescribed.All ChEIs have shown modest benefit on measures of cognitive function and activities of daily living.
Patients on ChEIs have shown slower declines on cognitive and functional measures than patients on placebo. However, ChEIs do not address the underlying cause of the degeneration of cholinergic neurons, which continues during the disease.
These are typically dose related and can be mitigated with slow up-titration to the desired maintenance dose. In addition, gastrointestinal side effects may be reduced by using the transdermal patch rather than the oral form of the drug. As antimuscarinic drugs are used for the treatment of incontinence, logically, ChEIs might exacerbate incontinence. One brief report has supported this hypothesis(32).ChEIs prescribed to treat dementia can provoke symptomatic bradycardia and syncope and precipitate fall-related injuries, including hip fracture. These reports have implications concerning the best practice when switching a patient from one ChEI to another in this class.
Reasons for switching might include undesirable side effects or an apparent lack of efficacy. Nonetheless, no published data are available to help clinicians know when it would be helpful to switch to another ChEI.The common practice of tapering a patient off one CNS-active medication before starting a new one should not be followed when changing ChEIs. Centrally acting anticholinergic medications should be avoided.It is not uncommon for patients to receive both ChEIs and anticholinergic agents, which counteract each other. Medications with anticholinergic effects, such as diphenhydramine, tricyclic antidepressants (eg, amitriptyline, nortriptyline), and oxybutynin (commonly used for bladder spasticity), can cause cognitive dysfunction. Therefore, a careful listing of the patient’s medications is important so that the physician can reduce the doses of, or ideally eliminate, all centrally acting anticholinergic agents.Cholinesterase inhibitors (ChEIs) are used to palliate cholinergic deficiency. All 4 currently approved ChEIs (ie, tacrine, donepezil, rivastigmine, galantamine) inhibit acetylcholinesterase (AChE) at the synapse (specific cholinesterase). Tacrine was the first agent that was approved for AD, but because of its potential to cause hepatotoxicity, it is now rarely used.Tacrine and rivastigmine also inhibit butyrylcholinesterase (BuChE). No data exist to indicate that this second mechanism is of clinical importance.Donepezil (Aricept, Aricept ODT)Donepezil is indicated for the treatment of dementia of the Alzheimer type. Donepezil has shown efficacy in patients with mild to moderate AD, as well as moderate to severe AD. It selectively inhibits acetylcholinesterase, the enzyme responsible for the destruction of acetylcholine, and improves the availability of acetylcholine.
Donepezil's long half-life provides a long duration of drug availability for binding at the receptor sites. There is no evidence to suggest that the underlying disease process of dementia is affected by administration of donepezil.Dosing recommendations for mild to moderate AD are 5-10 mg given once daily. Patients with moderate to severe AD can be given 10 or 23 mg once daily.Rivastigmine (Exelon, Exelon Patch)Rivastigmine is indicated for the treatment of mild to moderate dementia of the Alzheimer type. Rivastigmine is considered a pseudo-irreversible inhibitor of AChE.While the precise mechanism of rivastigmine's action is unknown, it is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine through reversible inhibition of its hydrolysis by cholinesterase.Galantamine (Razadyne, Razadyne ER)Galantamine is indicated for the treatment of mild to moderate dementia of the Alzheimer type.
There is no evidence that galantamine alters the course of the underlying dementing process. Tacrine inhibits AChE, the enzyme responsible for the destruction of acetylcholine, and improves the availability of acetylcholine.
This agent may be used alone or in combination with AChE inhibitors.Memantine (Namenda, Namenda XR)Namenda is approved for the treatment of moderate to severe dementia in patients with AD. Side effects include dizziness, confusion, headache, constipation, nausea, and agitation.B. Treatment of moderate to severe diseaseThe partial N -methyl-D-aspartate (NMDA) antagonist memantine (Namenda, Namenda XR) is believed to work by improving the signal-to-noise ratio of glutamatergic transmission at the NMDA receptor. Blockade of NMDA receptors by memantine is thought to slow the intracellular calcium accumulation and thereby help prevent further nerve damage.
This agent is approved by the FDA for treating moderate and severe AD.Several studies have demonstrated that memantine can be safely used in combination with ChEIs.
A variety of behavioral and pharmacologic interventions can alleviate clinical manifestations of AD, such as anxiety, agitation, depression, and psychotic behavior.
The effectiveness of such interventions ranges from modest and temporary to excellent and prolonged.

No specific agent or dose of individual agents is unanimously accepted for the wide array of clinical manifestations. Antidepressants have an important role in the treatment of mood disorders in patients with AD. Depression is observed in more than 30% of patients with AD, and it frequently begins before AD is clinically diagnosed.
However, a trial of 313 patients with moderate AD found that 24 months of treatment with valproate did not delay emergence of agitation or psychosis, did not slow cognitive or functional decline, and was associated A variety of experimental therapies have been proposed for AD. These include antiamyloid therapy, reversal of excess tau phosphorylation, estrogen therapy, vitamin E therapy, and free-radical scavenger therapy.
Studies are ongoing with agents that may prevent or reverse excess tau phosphorylation and thereby diminish formation of neurofibrillary tangles(43).Free-radical scavenger therapy has also attracted attention, because excess levels of free radicals in the brain are neurotoxic. Nonetheless, no study has demonstrated efficacy of free-radical scavengers in the treatment of the cognitive symptoms of AD.Various studies indicate that oxidative stress may be a part of the pathogenesis of AD. Therefore, use of vitamin E is not currently recommended.Transcranial magnetic stimulation (TMS) has been used to identify therapeutic targets in AD and to monitor the effects of pharmacologic agents, and both TMS and transcranial direct current stimulation are being explored for a possible therapeutic role in AD. However, evidence of therapeutic benefit from these modalities is highly preliminary(45).10. Herbal medicine is the bridage between complementary therapies &conventional treatmentIn all cultures, the origins of herbal medicine are lost in the mists of time. There is little doubt that humans used herbs for healing well before anything could be written about them. At some point in an advancing culture, written documents become the repository for knowledge that had been passed on from one generation to the next. Among the earliest such documents are those describing the religious beliefs of the people and those describing the medical practices.
Medical foods are dietary supplements intended to compensate specific nutritional problems caused by a disease or condition. Current western pharmacological approaches against neurodegeneration in dementia develop symptom-relieving and disease-modifying drugs. Current integrative and holistic approaches of Chinese medicine to discovering drugs for neurodegeneration in dementia include (1) single molecules from the herbs, (2) standardized extracts from a single herb, and (3) herbal formula with definite composition. At present, acetylcholinesterase inhibitors (AChEI) are the first group of drugs approved by the FDA to treat mild to moderate Alzheimer's disease. Most of these drugs such as huperzine and galanthamine are originally isolated from plants. However, AChE inhibitors have limited success as they only improve memory in mild dementia but cannot stop the process of neurodegeneration; while memantine possesses neuroprotective effects only with a little ability in memory enhancement. There has been a major rush among neuroscience research institutions and pharmaceutical firms worldwide to search for safer and more effective therapeutic agents for AD.However, mounting evidence obtained in vitro and in vivo, suggests that various traditionally used plants significantly affect key metabolic alterations culminating in AD-typical neurodegeneration. Beside synthetic drugs, a variety of AD related medicine originates from traditionally used plants. This herb has been subjected to numerous investigations regarding its potential in cognitive disorders. Standardized extracts, particularly EGb 761, derived from the plants’ leaves are successfully used as herbal drug for the improvement of cognitive and memory impairment. EGb 761 represents a prototype of plant extracts for attenuating Central Nervous System disorders, due to the fact that both flavonoids and terpenic lactones, which are partly also present in numerous other plant extracts, have been identified as the active principles in Ginkgo extracts as well as the ample experimental evidence on EGb 761’s protective efficiency in vitro and in vivo. The potential of EGb 761 to attenuate the cytotoxic effects of Alzheimer's related neurotoxic amyloid peptides when added to the culture medium was demonstrated not only in neuronal-like cell lines but also primary neurons, though with different efficiency.
The effects of oxidative stress were reduced in lymphocytes and brain cells derived of EGb 761-treated AD-transgenic and non-transgenic mice. Under the Dietary Supplement Health and Education Act of 1994, Gbe can be sold legally if it is not labeled or accompanied by any therapeutic or health claims. Herbal remedies can be labeled with descriptions of their role in affecting physiological structure or function, but must be labeled with a disclaimer that the product has not been evaluated by the FDA for cure, prevention, or treatment of a disease. Standardized ingredients of Gbe The extract utilized in medicine is standardized in a multi-step procedure designed to concentrate the desired active principles from the plant.
Ginkgolide B accounts for A?out 0.8% of the total extract and bilobalide accounts for A?out 3% of the extract.
Other constituents include proanthocyanadins, glucose, rhamnose, organic acids, D-glucaric acid and ginkgolic acid (at most 5 ppm ginkgolic acids).
Human Exposure: There is potential for ingestion of Gbe to a widespread consumer population, since this product is readily available without prescription at a cost highly competitive with prescription medications. The recommended dose ofGbe is 120 to 160 mg daily for persons with intermittent claudication and 240 mg daily for cerebrovascular insufficiency, early stage Alzheimer's disease, resistant depression, and impotence. Galantamine Galantamine is an alkaloid known form several members of the Amaryllis family (Amaryllidaceae), and the idea for developing a medical product for AD from these species seems to be based on the local use of one of these species in a remote part of Europe. It has become an important therapeutic options used to slow down the process of neurological degeneration in AD. Its development from little known observational studies in the Caucasus Mountains (Southern Russia), to the use of this drug in Eastern European countries (esp. Bulgaria) in the treatment of poliomyelitis and ultimately to the recent introduction onto Western markets in the treatment of AD. Galantamine was first isolated from snowdrop (Galanthus spp.) but today it is obtained from Narcissus spp. According to unconfirmed reports, in the 1950s, a Bulgarian pharmacologist noticed the use of the common snowdrop growing in the wild by people who were rubbing it on their foreheads to ease nerve pain. Also, some of the earlier publications indicate the extensive use of snowdrop in Eastern Europe, such as Romania, Ukraine, the Balkan Peninsula, and in the Eastern Mediterranean countries. However, Mashkovsky and Kruglikova-Lvov published the first work that establishes the acetylcholine esterase inhibiting properties of galantamine isolated from Galanthusworonowii. Poliomyelitis was one of the first indications for galantamine, especially in the Eastern and Central European, since the compound enhances nerve impulse transmission at the synapse. Studies indicating blood–brain barrier penetration of the alkaloid pioneer the development of CNS-related indications. Based on the knowledge of galantamine in both the peripheral and central nervous system, many countries in Eastern Europe used it as an acknowledged treatment in Myasthenia gravis and muscular dystrophy, residual poliomyelitis paralysis symptoms, trigeminal neurologica, and other forms of neuritis. A crucial step for the success of galantamine as a medicine against AD was based on the synthesis developed in the mid-1990s. The scientific rationale for using cholinesterase inhibitors in the management of AD is based on the cholinergic hypothesis.
Impairment of the central cholinergic system represents one hallmark of AD, which is characterized by loss of cholinergic neurons in the forebrain and a marked decrease in the activity of choline acetyltransferase. Panax ginseng roots are traditionally taken orally as adaptogens, aphrodisiacs, nourishing stimulants, and in the treatment of sexual dysfunction in men. The fresh root, can be directly chewed, or soaked in various wines for a period of time before drinking or chewing. However, usually ginseng is used at subclinical doses for a short period and as such; it does not produce measurable medicinal effects. Panax notoginseng is widely used in traditional Chinese medicine (TCM) to improve learning and memory. It is popular in cultivation in Europe, and valued for its wide, green, shiny leaves, whicht provide good ground-cover and contrast with the leaves of the commonly grown snowdrop G.
It is primarily found around the eastern Black Sea coast in the ancient provinces of Colchis and Lazistan (the Euxine Province).
It occurs at 70–1,400 metres above sea level, in stony and rocky spots (on calcareous rocks, in gorges, on stony slopes and on scree), on river banks, in scrub and at forest margins, and sometimes as an epiphyte or on fallen tree trunks, rooting in moss(46-48).15.
2005 indicate that cannabinoids succeed in preventing the neurodegenerative process occurring in the AD,"(50). Follow up studies by investigators demonstrated that the administration of the nonpsychotropic plant cannabinoid cannabidiol (CBD) also mitigated memory loss in a mouse model of the disease(51).Investigators at the Scripps Research Institute in California in 2006 reported that THC (Tetrahydrocannabinol (THC) is the active chemical in cannabis and is one of the oldest hallucinogenic drugs known) inhibits the enzyme responsible for the aggregation of amyloid plaque — the primary marker for AD — in a manner "considerably superior" to approved Alzheimer's drugs such as donepezil and tacrine. The investigators’s results provide a mechanism whereby the THC molecule can directly impact AD pathology," researchers concluded. 2007, reported that rats treated with the compound experienced a 50 percent improvement in memory and a 40 to 50 percent reduction in inflammation compared to controls(53).
Previous preclinical studies have demonstrated that cannabinoids can prevent cell death by anti-oxidation. Some experts believe that cannabinoids' neuroprotective properties could also play a role in moderating AD (54). 2007, reported that "Cannabinoids offer a multi-faceted approach for the treatment of AD by providing neuroprotection and reducing neuroinflammation, whilst simultaneously supporting the brain's intrinsic repair mechanisms by augmenting neurotrophin expression and enhancing neurogenesis. Manipulation of the cannabinoid pathway offers a pharmacological approach for the treatment of AD that may be efficacious than current treatment regimens (55). In addition to potentially modifying the progression of AD, clinical trials also indicate that cannabinoid therapy can reduce agitation and stimulate weight gain in patients with the disease. Curcumin (diferuloylmethane)Curcumin (diferuloylmethane), a polyphenol compound responsible for the bright yellow color of turmeric, is believed to be the principal pharmacological agent. In addition to curcumin, turmeric contains the curcuminoids atlantone, bisdemethoxycurcumin, demethoxycurcumin, diaryl heptanoids, and tumerone.
Other constituents include sugars, resins, proteins, vitamins, and minerals (including iron and potassium).Due to various effects of curcumin, such as decreased Beta-amyloid plaques, delayed degradation of neurons, metal-chelation, anti-inflammatory, antioxidant and decreased microglia formation, the overall memory in patients with AD has improved(61).
Researchers found that curcumin may help the macrophages to clear the amyloid plaques found in Alzheimer's disease. Curcumin was treated with macrophages in blood taken from nine volunteers: six AD patients and three healthy controls. The AD patients, whose macrophages were treated with curcumin, when compared with patients whose macrophages were not treated with curcumin, showed an improved uptake and ingestion of the plaques. These compounds may protect the cells from beta A(1-42) insult through antioxidant pathways. Other animal studies of AD also suggest that curcumin may reduce levels of amyloid and oxidized proteins and prevent cognitive deficits (65). One alternative mechanism of action for these effects suggested by Baum et al (65), is metal chelation, which may reduce amyloid aggregation or oxidative neurotoxicity.
Since curcumin more readily binds the redox-active metals and than the redox-inactive, curcumin might exert a net protective effect against beta toxicity or might suppress inflammatory damage by preventing metal induction of NF-kappaB.
Mouse studies that evaluated the effects of dietary curcumin on inflammation, oxidative damage, and plaque pathology demonstrated that both low and high doses of curcumin significantly lowered oxidized proteins and interleukin-1beta, which is a proinflammatory cytokine elevated in the brains of these mice (66).
Low-dose but not high-dose curcumin treatment has been shown to reduce the astrocytic marker GFAP and significantly decrease insoluble (A?), soluble Abeta, and plaque burden by 43-50%. Huperzine A (Qian Ceng Ta)Huperzine A, shows promise for enhancing memory and protecting cognitive functions and may improve cognition in AD.Huperzine-Ais a new supplement derived from an ancient traditional Chinese herbal medicine that offers hope to those suffering from AD and other age-related mental conditions(67).

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