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Herbs & Plants

Yuan Zhi

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Botanical Name : Polygala tenuifolia
Family: Polygalaceae
Genus: Polygala
Species: P. tenuifolia
Kingdom: Plantae
Order: Fabales

Common Names : Chinese Senega, Yuan Zhi,polygala, Chinese senega root,Thinleaf Milkwort Root,Polygala root,thin-leaf milkwort root

Other Names:Chinese Senega, Flax, Klapperschlangen, Milkwort, Mountain Polygala, Polygalae radix, Rattlesnake Root, Senaga Snakeroot, Seneca, Seneca Snakeroot, Senega, Senega Snakeroot, Seneka, Snake Root. Polygala glomerata; Polygala japonica; Polygala reinii; Polygala senega, synonym Polygala senega latifolia; Polygala tenuifolia.

Habitat : Polygala tenuifolia is native to  E. Asia – Korea, Mongolia, Manchuria. Grows in the  Hillsides, roadsides and meadows. Dry meadows and stony slopes.

Description:
Polygala tenuifolia is a perennial herb,  growing to 0.2 m (0ft 8in) by 0.2 m (0ft 8in).  It is hardy to zone 6. The flowers are hermaphrodite (have both male and female organs)

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The plant prefers light (sandy), medium (loamy) and heavy (clay) soils and requires well-drained soil.The plant prefers acid, neutral and basic (alkaline) soils..It can grow in semi-shade (light woodland) or no shade.It requires moist soil.

Cultivation:
Prefers a moderately fertile moisture-retentive well-drained soil, succeeding in full sun if the soil remains moist throughout the growing season, otherwise it is best in semi-shade. Dislikes shade according to another report. Plants are hardy to at least -15°c.

Propagation  :
Seed – sow spring or autumn in a cold frame. When they are large enough to handle, prick the seedlings out into individual pots and grow them on in the greenhouse for their first winter. Plant them out into their permanent positions in late spring or early summer, after the last expected frosts. Division. Cuttings of young shoots in a frame in late spring.

Edible Uses
Edible Parts: Leaves;  Root.

Young leaves – cooked. Root – cooked. The core is removed and the root is boiled in several changes of water.

Medicinal Uses :
Cardiotonic;  ExpectorantHaemolytic;  Kidney;  Sedative;  Tonic.

Yuan Zhi is used primarily as an expectorant. It is one of the 50 fundamental herbs used in traditional Chinese medicine, where it is called yuan zhi .

Yuan Zhi contains triterpenoid saponins, these promote the clearing of phlegm from the bronchial tubes. The plant is used mainly as an expectorant and stimulant to treat bronchial asthma, chronic bronchitis and whooping cough. The root is antibacterial, cardiotonic, cerebrotonic, expectorant, haemolytic, hypotensive, sedative and tonic. It acts mainly as a tonic for the heart and kidney energies. It is taken internally in the treatment of coughs with profuse phlegm, bronchitis, insomnia, palpitations, poor memory, anxiety, depression and nervous tension. Externally it is used to treat boils and carbuncles. The root is harvested in the autumn and dried for later use. The leaves are used as a tonic for the kidneys.

Medical study:
A randomized, double-blind, placebo-controlled, parallel-group study of the extract of dried roots of Polygala tenuifolia in healthy adults produced memory-enhancing effects. A similar trial with elderly humans also found significant cognitive improvement.

A number of in vitro experiments have examined the use of the herb in Alzheimer’s disease, memory disorder, depression, amnesia, cognitive defects, neurotoxicity, degenerative disease,and dementia among others. Results have been encouraging

Known Hazards : Although no specific mention has been seen for this species, at least one member of this genus is said to be poisonous in large quantities.

Disclaimer:The information presented herein is intended for educational purposes only. Individual results may vary, and before using any supplements, it is always advisable to consult with your own health care provider

Resources:
http://www.pfaf.org/user/Plant.aspx?LatinName=Polygala+tenuifolia
http://www.plantsystematics.org/imgs/mmy8/r/Polygalaceae_Polygala_tenuifolia_25750.html
http://www.mdidea.com/products/new/new09801.html
http://en.wikipedia.org/wiki/Polygala_tenuifolia

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Categories
Ailmemts & Remedies

Huntington’s Disease

Definition:
Huntington’s disease (also referred to in more formal medical research as Huntington Disease) is an hereditary neurological disorder of the central nervous system that causes progressive degeneration of cells in the brain, slowly impairing a person’s ability to walk, think, talk and reason.

Most people with Huntington’s disease develop signs and symptoms in their 40s or 50s, but the onset of disease may be earlier or later in life. When disease onset begins before age 20, the condition is called juvenile Huntington’s disease. Earlier onset often results in a somewhat different presentation of symptoms and faster disease progression.

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Medications are available to help manage the symptoms of Huntington’s disease, but treatments can’t prevent the physical, mental and behavioral decline associated with the condition.

It was first described in 1872 by an American doctor, George Huntington, who studied an extended family in Long Island affected by the condition.

Symptoms:
Symptoms of Huntington’s disease commonly become noticeable between the ages of 35 and 44 years, but they can begin at any age from infancy to old age. In the early stages, there are subtle changes in personality, cognition, and physical skills. The physical symptoms are usually the first to be noticed, as cognitive and psychiatric symptoms are generally not severe enough to be recognized on their own at the earlier stages. Almost everyone with Huntington’s disease eventually exhibits similar physical symptoms, but the onset, progression and extent of cognitive and psychiatric symptoms vary significantly between individuals.

The most characteristic initial physical symptoms are jerky, random, and uncontrollable movements called chorea. Chorea may be initially exhibited as general restlessness, small unintentionally initiated or uncompleted motions, lack of coordination, or slowed saccadic eye movements. These minor motor abnormalities usually precede more obvious signs of motor dysfunction by at least three years. The clear appearance of symptoms such as rigidity, writhing motions or abnormal posturing appear as the disorder progresses. These are signs that the system in the brain that is responsible for movement is affected.[6] Psychomotor functions become increasingly impaired, such that any action that requires muscle control is affected. Common consequences are physical instability, abnormal facial expression, and difficulties chewing, swallowing and speaking. Eating difficulties commonly cause weight loss and may lead to malnutrition.  Sleep disturbances are also associated symptoms. Juvenile HD differs from these symptoms in that it generally progresses faster and chorea is exhibited briefly, if at all, with rigidity being the dominant symptom. Seizures are also a common symptom of this form of HD.

Cognitive abilities are impaired progressively. Especially affected are executive functions which include planning, cognitive flexibility, abstract thinking, rule acquisition, initiating appropriate actions and inhibiting inappropriate actions. As the disease progresses, memory deficits tend to appear. Reported impairments range from short-term memory deficits to long-term memory difficulties, including deficits in episodic (memory of one’s life), procedural (memory of the body of how to perform an activity) and working memory. Cognitive problems tend to worsen over time, ultimately leading to dementia. This pattern of deficits has been called a subcortical dementia syndrome to distinguish it from the typical effects of cortical dementias e.g. Alzheimer‘s disease.

Reported neuropsychiatric manifestations are anxiety, depression, a reduced display of emotions (blunted affect), egocentrism, aggression, and compulsive behavior, the latter of which can cause or worsen addictions, including alcoholism, gambling, and hypersexuality.  Difficulties in recognizing other people’s negative expressions have also been observed. Prevalence of these symptoms is also highly variable between studies, with estimated rates for lifetime prevalence of psychiatric disorders between 33% and 76%.  For many sufferers and their families these symptoms are among the most distressing aspects of the disease, often affecting daily functioning and constituting reason for institutionalisation. Suicidal thoughts and suicide attempts are more common than in the general population.

Mutant Huntingtin is expressed throughout the body and associated with abnormalities in peripheral tissues that are directly caused by such expression outside the brain. These abnormalities include muscle atrophy, cardiac failure, impaired glucose tolerance, weight loss, osteoporosis and testicular atrophy

Reported prevalences of behavioral and psychiatric symptoms in Huntington’s disease :
Irritability 38–73%
Apathy 34–76%
Anxiety 34–61%
Depressed mood 33–69%
Obsessive and compulsive 10–52%
Psychotic 3–11%

Causes:
Huntington’s disease is caused by a single defective gene on chromosome 4. This leads to damage of the nerve cells in areas of the brain including the basal ganglia and cerebral cortex, and to the gradual onset of physical, mental and emotional changes.

The Huntington’s Disease Association estimates between 6,500 and 8,000 people in the UK have the disease.

The tragedy is that by the time symptoms appear, the person has often had a family and may have passed on the gene to their children. Each person whose parent has Huntington’s disease has a 50 per cent chance of inheriting the gene, and everyone who inherits the gene will at some stage develop the disease.

In three per cent of cases, there’s no family history of Huntington’s disease and the genetic fault may be a new mutation.

The disease can’t be prevented from developing if someone has the faulty gene. To inherit the illness, the gene only has to come from one parent, making it autosomal dominant.

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The gene for Huntington’s disease can be detected with a blood test, which is available to those aged over 18, before symptoms begin. This can determine whether someone has the faulty gene and help them in their family planning

Risk Factors:
If one of your parents has Huntington’s disease, you have a 50 percent chance of developing the disease. In rare cases, you may develop Huntington’s disease without having a family history of the condition. Such an occurrence may be the result of a genetic mutation that happened during your father’s sperm development.

Complications:
After the onset of Huntington’s disease, a person’s functional abilities gradually worsen over time. The rate of disease progression and duration varies. The time from disease onset to death is often about 10 to 30 years. Juvenile onset usually results in death in fewer than 15 years.

The clinical depression associated with Huntington’s disease may increase the risk of suicide. Some research suggests that the greater risk of suicide occurs before a diagnosis is made and in middle stages of the disease when a person has begun to lose independence.

Eventually, a person with Huntington’s disease requires help with all activities of daily living and care. Late in the disease, he or she will likely be confined to a bed and unable to speak. However, a person’s understanding of surroundings and interactions remain intact for a long time.

Common causes of death include:

*Pneumonia or other infections
*Injuries related to falls
*Complications related to the inability to swallow

Diagnosis:
Medical diagnosis of the onset of HD can be made following the appearance of physical symptoms specific to the disease. Genetic testing can be used to confirm a physical diagnosis if there is no family history of HD. Even before the onset of symptoms, genetic testing can confirm if an individual or embryo carries an expanded copy of the trinucleotide repeat in the HTT gene that causes the disease. Genetic counseling is available to provide advice and guidance throughout the testing procedure, and on the implications of a confirmed diagnosis. These implications include the impact on an individual’s psychology, career, family planning decisions, relatives and relationships. Despite the availability of pre-symptomatic testing, only 5% of those at risk of inheriting HD choose to do so

Clinical:
A physical examination, sometimes combined with a psychological examination, can determine whether the onset of the disease has begun. Excessive unintentional movements of any part of the body are often the reason for seeking medical consultation. If these are abrupt and have random timing and distribution, they suggest a diagnosis of HD. Cognitive or psychiatric symptoms are rarely the first diagnosed; they are usually only recognized in hindsight or when they develop further. How far the disease has progressed can be measured using the unified Huntington’s disease rating scale which provides an overall rating system based on motor, behavioral, cognitive, and functional assessments. Medical imaging, such as computerized tomography (CT) and magnetic resonance imaging (MRI), only shows visible cerebral atrophy in the advanced stages of the disease. Functional neuroimaging techniques such as fMRI and PET can show changes in brain activity before the onset of physical symptoms.

Grenetic:
Because HD follows an autosomal dominant pattern of inheritance, there is a strong motivation for individuals who are at risk of inheriting it to seek a diagnosis. The genetic test for HD consists of a blood test which counts the numbers of CAG repeats in each of the HTT alleles.[38] A positive result is not considered a diagnosis, since it may be obtained decades before the symptoms begin. However, a negative test means that the individual does not carry the expanded copy of the gene and will not develop HD.

A pre-symptomatic test is a life-changing event and a very personal decision. The main reason given for choosing testing for HD is to aid in career and family decisions. Over 95% of individuals at risk of inheriting HD do not proceed with testing, mostly because there is no treatment. A key issue is the anxiety an individual experiences about not knowing whether they will eventually develop HD, compared to the impact of a positive result.  Irrespective of the result, stress levels have been found to be lower two years after being tested, but the risk of suicide is increased after a positive test result. Individuals found to have not inherited the disorder may experience survivor guilt with regard to family members who are affected. Other factors taken into account when considering testing include the possibility of discrimination and the implications of a positive result, which usually means a parent has an affected gene and that the individual’s siblings will be at risk of inheriting it. Genetic counseling in HD can provide information, advice and support for initial decision-making, and then, if chosen, throughout all stages of the testing process. Counseling and guidelines on the use of genetic testing for HD have become models for other genetic disorders, such as autosomal dominant cerebellar ataxias. Presymptomatic testing for HD has also influenced testing for other illnesses with genetic variants such as polycystic kidney disease, familial Alzheimer’s disease and breast cancer

Embryonic:
Embryos produced using in vitro fertilisation may be genetically tested for HD using preimplantation genetic diagnosis. This technique, where a single cell is extracted from a 4 to 8 cell embryo and then tested for the genetic abnormality, can then be used to ensure embryos with affected HTT genes are not implanted, and therefore any offspring will not inherit the disease. It is also possible to obtain a prenatal diagnosis for an embryo or fetus in the womb.

Differential diagnosis:
About 90% of HD diagnoses based on the typical symptoms and a family history of the disease are confirmed by genetic testing to have the expanded trinucleotide repeat that causes HD. Most of the remaining are called HD-like disorders.  Most of these other disorders are collectively labelled HD-like (HDL). The cause of most HDL diseases is unknown, but those with known causes are due to mutations in the prion protein gene (HDL1), the junctophilin 3 gene (HDL2), a recessively inherited HTT gene (HDL3—only found in one family and poorly understood), and the gene encoding the TATA box-binding protein (HDL4/SCA17). Other autosomal dominant diseases that can be misdiagnosed as HD are dentatorubral-pallidoluysian atrophy and neuroferritinopathy. There are also autosomal recessive disorders that resemble sporadic cases of HD. Main examples are chorea acanthocytosis, pantothenate kinase-associated neurodegeneration and X-linked McLeod syndrome

Treatment:
There’s no cure, but supportive care can ease many symptoms and help a person with Huntington’s disease, and their family, lead as normal a life as possible.

Drugs can relieve symptoms of involuntary movements, depression and mood swings. Speech therapy can help improve speech and swallowing problems. A high-calorie diet can help maintain weight and improve symptoms such as involuntary movement and behavioural problems.

Cognitive changes often result in loss of enthusiasm, initiative and organisational skills, which can make multi-tasking difficult. Constant nursing care is needed in the later stages of the disease and support for carers is important, too.

Secondary illnesses, such as pneumonia, are often the cause of death.

There’s extensive research into possible treatments for Huntington’s disease. One technique is the use of transplants of foetal brain cells, which appear in some cases to repair and rejuvenate the damaged area.

Meanwhile, researchers at the University of Leeds have found that one of the body’s naturally occurring proteins is causing some of the disruption that occurs in the brains of those with Huntington’s, and its effects may be modified by using drugs that are already being used to help cancer patients. But it is likely to be years, if at all, before these developments result in an effective treatment.

Prognosis:
The length of the trinucleotide repeat accounts for 60% of the variation in the age of onset and the rate of progression of symptoms. A longer repeat results in an earlier age of onset and a faster progression of symptoms. For example, individuals with a trinucleotide repeat greater than sixty repeats often develop the disease before twenty years of age, and those with less than forty repeats may not develop noticeable symptoms. The remaining variation is due to environmental factors and other genes that influence the mechanism of the disease.

Life expectancy in HD is generally around 20 years following the onset of visible symptoms.  Most of the complications that are life-threatening result from muscle coordination issues, or to a lesser extent from behavioural changes resulting from the decline in cognitive function. The largest risk is pneumonia, which is the cause of death of one-third of those with HD. As the ability to synchronise movements deteriorates, difficulty clearing the lungs and an increased risk of aspirating food or drink both increase the risk of contracting pneumonia. The second greatest risk is heart disease, which causes almost a quarter of fatalities of those with HD. Suicide is the next greatest cause of fatalities, with 7.3% of those with HD taking their own lives and up to 27% attempting to do so. It is unclear to what extent suicidal thoughts are influenced by psychiatric symptoms, as they may be considered to be a response of an individual to retain a sense of control of their life or to avoid the later stages of the disease.  Other associated risks include choking, physical injury from falls, and malnutrition.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose

Resources:
http://www.bbc.co.uk/health/physical_health/conditions/huntingtons1.shtml
http://en.wikipedia.org/wiki/Huntington’s_disease
http://www.mayoclinic.com/health/huntingtons-disease/DS00401

http://www.healthtree.com/articles/huntingtons-disease/causes/

http://www.bothbrainsandbeauty.com/academic-discussions/huntingtons-disease-991

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Ailmemts & Remedies

Binswanger’s Disease

Alternative Name: Subcortical vascular dementia.

Definition:
Binswanger’s disease is a form of small vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents itself in 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.

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A  form of multi-infarct dementia caused by damage to the white brain matter.

Binswanger’s disease is a particular type of atherosclerosis-related dementia, in which there are widespread, microscopic areas of damage to the white matter below the outer layer or cortex of the brain. This is called subcortical dementia and produces a particular pattern of symptoms which is somewhat different to other types of dementia.

The disease may develop gradually or seem to be triggered or rapidly aggravated by a stroke or other event that leads to brain damage.

It was described by Otto Binswanger in 1894, and Alois Alzheimer first used the phrase “Binswanger’s disease” in 1902.  However, Olszewski is credited with much of the modern-day investigation of this disease which began in 1962

Symptoms:
Binswanger’s disease affects the speed at which the brain can process information and this typically causes problems with higher brain functions such as:

•Organisation
•Planning
•Decision making
•Attention
•Concentration (all of which impinge on intellectual function)
•Mood (typically apathy, irritability, and depression)
•Behaviour
Memory loss can occur but is not usually as bad as in other forms of dementia such as Alzheimer’s, while a feature known as psychomotor slowness (where a person takes longer than normal to turn a thought into an action) is common in Binswanger’s disease.

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There may also be changes in speech, an unsteady gait, shaking similar to that seen in Parkinson’s disease, clumsiness or frequent falls and loss of bladder control. These symptoms are not always present in all patients and may sometimes appear only as a passing phase. Seizures may also occur.

Patients usually show other signs of atherosclerosis and cardiovascular disease such as:

•Raised blood pressure
•Stroke
•Blood abnormalities
•Disease of the large blood vessels in the neck
•Disease of the heart valves
Brain scans such as CT scans or magnetic resonance imaging (MRI) show a characteristic pattern in Binswanger’s disease.

Causes:

Atherosclerosis, a disease process that narrows the blood vessels and cuts off the blood supply to the neurons or nerve cells of the brain, causing death of those cells, is a common cause of dementia.

Binswanger’s disease is a particular type of atherosclerosis-related dementia, in which there are widespread, microscopic areas of damage to the white matter below the outer layer or cortex of the brain. This is called subcortical dementia and produces a particular pattern of symptoms which is somewhat different to other types of dementia.

Diagnosis:

Binswanger’s disease can usually be diagnosed through a CT scan, MRI, and a proton MR spectrography. Indications include infarctions, lesions, or loss of intensity of central white matter and enlargement of ventricles, and leukoaraiosis or white matter atrophy. click & see

Click to see the picture

CT Brain Scan showing active NCC (left) and lacunar infarction on the head of the caudate nucleus (right) and lecoara.

Presentation:

Leukoaraiosis (LA) are white matter changes that are common in Binswanger’s Disease. However, LA can be found in many different diseases and even in the general population, especially in people older than 65 years of age.

There is controversy whether LA and mental deterioration actually have a cause and effect relationship. Recent research is showing that different types of LA can affect the brain differently, and that proton MR spectroscopy would be able to distinguish the different types more effectively and better diagnosis and treat the issue.[8] Because of this information, white matter changes indicated by a MRI or CT cannot alone diagnose Binswanger’s disease, but can aid to a bigger picture in the diagnosis process. There are many diseases similar to Binswanger’s disease including CADASIL syndrome and Alzheimer’s disease which makes this specific type of white matter damage hard to diagnose.Binswanger’s disease is best when diagnosed of a team by experts including a neurologist and psychiatrist to rule out other psychological or neurological problems. Because doctors must successfully detect enough white matter alterations to accompany dementia as well as an appropriate level of dementia, two separate technological systems are needed in the diagnosing process.

Technology:

Much of the major research today is done on finding better and more efficient ways to diagnose this disease. Many researchers have divided the MRIs of the brain into different sections or quadrants. A score is given to each section depending on how severe the white matter atrophy or leukoaraiosis is. Research has shown that the higher these scores, the more of a decrease in processing speed, executive functions, and motor learning tasks. Other researchers have begun using computers to calculate the percentage of white matter atrophy by counting the hyper-intense pixels of the MRI. These and similar reports show a correlation between the amount of white matter alterations and the decline of psychomotor functions, reduced performance on attention and executive control. One recent type of technology is called susceptibility weighted imaging (SWI) which is a magnetic resonance technique which has an unusually high degree of sensitivity and can better detect white matter alternations.

Recently a Mini Mental Test (MMT) has been created to accurately and quickly assess cognitive impairment due to vascular dementia across different cultures. Binswanger’s disease has been shown to be the most severe impairment of all of the vascular dementia.


Treatment:

There is no specific treatment for Binswanger’s disease. What treatment there is consists of keeping associated symptoms under control and supporting the patient with their activities of daily living such as dressing, washing and preparing meals.

Medications may be used to treat symptoms such as depression, or generally treat arterial disease and its effects throughout the body (so helping to preserve blood flow to the brain and delay the progression of Binswanger’s).

Specific drugs called “cognitive enhancers” used generally in dementia may be given but the results with them are variable and many people get little benefit.

It has been shown that current Alzheimer’s medication, Aricept, may help Binswanger’s Disease patients as well. Aricept increases the acetocholine in the brain through a choline esterase inhibitor which deactivates the enzyme that breaks down acetocholine. Alzheimer as well as Binswanger patients have low levels of acetocholine and this helps to restore the normal levels of neurotransmitters in the brain. This drug may improve memory, awareness, and the ability to function. If no medical interception of the disease is performed then the disease will continue to worsen as the patient ages due to the continuing atrophy of the white matter from whatever was its original cause.

You may click to see :Homoeopathy and  Binswanger’s disease

Prognosis:
Binswanger’s disease has no cure and patients with the disorder usually die within five years of its onset.
The best way to manage the vascular risk factors that contribute to poor perfusion in the brain is to treat the cause, such as chronic hypertension or diabetes.

Disclaimer: This information is not meant to be a substitute for professional medical advise or help. It is always best to consult with a Physician about serious health concerns. This information is in no way intended to diagnose or prescribe remedies.This is purely for educational purpose.

Resources:

http://en.wikipedia.org/wiki/Binswanger’s_disease
http://www.bbc.co.uk/health/physical_health/conditions/binswangers_disease.shtml

Binswanger’s disease or Binswager’s Dementia

http://www.ispub.com/ostia/index.php?xmlFilePath=journals/ijn/vol2n1/bins.xml

http://www.walgreens.com/marketing/library/contents.html?docid=000002&doctype=10

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News on Health & Science

Memory Foggy? 5 Signs It’s Not Serious

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It’s natural to feel nervous when you forget something, knowing that Alzheimer’s disease now affects 5.3 million Americans.  But a memory slip doesn’t always mean the worst. According to KPHO, the following five situations point toward normal, age-related memory loss.

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1.Lapses Don’t Interfere With Everyday Life
Slowed recall of information from time to time is normal — erverybody forgets stuff.  What’s not normal is when memory impairment interferes with your ability to get through the day.

2.You See an Improvement After ‘Brain Training’
Dementia is not a problem of retrieving old memories so much as it is is an inability to form new ones. If you can still learn new things, you’re still forming new memories.

3.You’ve Just Started A New Medication
Drug side effects are one of the more common causes of memory trouble.

4.Nobody Else Seems To Notice Anything’s Amiss
Usually, there’s a lot of family friction around the kind of memory loss that predates a diagnosis — arguments over who neglected to do something, missed appointments, or forgotten messages.

5.You’re Forgetful When Stressed, Sleep Deprived or Multitasking
A stressed brain is not the same thing as a demented brain.

Source: KPHO December 9, 2010

Posted By:  Dr. Mercola | December 30 2010

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Healthy Tips

Walking ‘Could Ward off Dementia and Mental Decline’

Elderly people who get about by walking are less likely to suffer mental decline or even dementia, a study says.

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Brain scans revealed that older people walking between six and nine miles a week appeared to have more brain tissue in key areas.

The Pittsburgh University study of 299 people suggested they had less “brain shrinkage“, which is linked to memory problems.

The research was reported in the journal Neurology.

The volunteers, who had an average age of 78, were checked for signs of “cognitive impairment” or even dementia.

The Pittsburgh team also had access to brain scan results from four years previously which measured the amount of “grey matter” in their brains.

Brain health

This is found at various parts of the brain and is known to diminish in many people as they get older.

Each of them had been quizzed in their 60s about the number of city blocks they walked each week as part of their normal routine.

The results showed that those who walked at least 72 blocks – six to nine miles – a week had a greater volume of grey matter.

Four years after the scans, 40% of the group had measurable cognitive impairment or even dementia.

Those who walked the most were half as likely to have these problems compared with those who walked the least.

Dr Kirk Erickson, who led the study, said: “If regular exercise in midlife could improve brain health and improve thinking and memory in later life, it would be one more reason to make regular exercise in people of all ages a public health imperative.”

Susanne Sorensen, from the Alzheimer’s Society, said that the study was further evidence that a healthy heart could lead to a healthy brain.

She added: “One of the benefits of this research is that it eliminates the impact other socio-economic factors may play and focuses specifically on walking rather than exercise more generally.

“Although a link has been found between lack of exercise and brain shrinkage, we need more research to find out why physical activity may affect the brain.

“The best way to reduce your risk is to take regular exercise, eat healthily, don’t smoke and get your blood pressure and cholesterol checked.”


Source
: BBC News

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