Amazing Benefits of Drinking Tea Decreases Dementia/Alzheimer’s by 50%

Thanks to its high levels of antioxidants, drinking tea is linked to lower risk of diabetes, heart disease, and cancer.

Now, a new study finds its benefits don’t end there. It found that tea drinkers cut their chances of dementia in half.

And if Alzheimer’s runs in your family, tea is even more protective. People who inherit ApoE4, the so-called “Alzheimer’s gene,” reduce their risk 86% by drinking tea regularly.

Researchers from the Yon Loo Lin School of Medicine in Singapore followed 957 adults for more than five years. All the subjects were 55 or older.

During the study, 72 of the participants developed some form of cognitive decline. Scientists found that people who drank tea at least once a day had a 50% lower risk of memory problems.

Those who drank green tea reduced their risk by 43%. People who drank black or oolong tea reduced their risk by 53%.

This is particularly important for people with a genetic risk for Alzheimer’s. Having one copy of the ApoE4 gene gives you a 25% chance of developing Alzheimer’s. People with two copies of the gene (about 2% of the population) have a nine in 10 chance.

Dr. Lei said tea’s brain-protective effects are “due to the bioactive compounds in tea leaves, such as catechins, theaflavins, thearubigins, and L-theanine.3

“These compounds exhibit anti-inflammatory and antioxidant potential and other bioactive properties that may protect the brain from vascular damage and neurodegeneration,” he said.

Tea brewed directly from the leaves has more beneficial compounds than tea made using tea bags, researchers said.

And if you are worried about Alzheimer’s, there is something else you should know…

The decades’ worth of research on one natural herb is impressive to say the least. And Big Pharma knows it… They’re trying to turn this extract into a drug. Go here to get all the details.

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Sense of Smell vs. Dementia

Older people with a poor sense of smell have a greater chance of developing Alzheimer’s and other forms of dementia, US research has shown.

The discovery raises the prospect of using “sniffing sticks” to flag individuals needing closer monitoring in the next five years.

Though humans lack the acute sense of some animals such as dogs, they can distinguish up to a trillion different odors.

The brain’s ability to sort and recognize smells may provide a way of spotting early damage caused by neurodegenerative disease, the research suggests.

But experts warned that impaired smell detection was not always a symptom of early dementia.

Almost 3000 adults aged 57 to 85 took part in the long-term US study, which involved waving “sniffing sticks” with various smell flavors in front of their noses.

Those with a “normal” sense of smell could identify at least four out of five common odors.

Compared with this group, people who failed the test were more than twice as likely to develop dementia five years later.

The vast majority of those tested, 78 per cent, had a “normal” sense of smell and could accurately identify the scents.

But 14 per cent could name just three out of five, 5 per cent could identify only two, and 2 per cent could recognize only one.

Just 1 per cent of participants were not able to name a single smell.

Five years after the initial test, almost every participant who was unable to name any of the smells had been diagnosed with dementia.

Nearly 80 per cent of those who provided only one or two correct answers had developed the condition.

There was a dose-dependent effect, the study found, with dementia rates rising in step with increasingly poor smell sense.

Lead scientist Professor Jayant Pinto, from the University of Chicago, said: “These results show that the sense of smell is closely connected with brain function and health.

“We think smell ability specifically, but also sensory function more broadly, may be an important early sign, marking people at greater risk for dementia.

“Loss of the sense of smell is a strong signal that something has gone wrong and significant damage has been done. This simple smell test could provide a quick and inexpensive way to identify those who are already at high risk.”

The findings are reported in the Journal of the American Geriatrics Society.

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2017 Dementia/Alzheimer’s Information

Dementiachronic, usually progressive deterioration of intellectual capacity associated with the widespread loss of nerve cells and the shrinkage of brain tissue. Dementia is most commonly seen in the elderly (senile dementia), though it is not part of the normal aging process and can affect persons of any age. In 2005 researchers reported that some 24.3 million people worldwide were living with dementia. In 2010 this figure rose to an estimated 35.6 million, a number that was expected to double by 2030, in part because of anticipated increases in life expectancy in many countries.

Histopathologic image of neuritic plaques in the cerebral cortex in a patient with Alzheimer …

The most common irreversible dementia is Alzheimer disease. This condition often begins with memory loss or with subtle impairments in other cognitive functions. These changes may manifest initially as simple absentmindedness or forgetfulness or as minor problems with judgment, language, or perception. As dementia progresses, memory loss and cognitive impairment broaden in scope until the individual can no longer remember basic social and survival skills or function independently. Language, spatial or temporal orientation, judgment, perception, and other cognitive capacities decline, and personality changes may occur. Dementia is also present in other degenerative brain diseases, including Pick disease and Parkinson disease.

The second most common cause of dementia is hypertension (high blood pressure) or other vascular conditions. This type of dementia, called multi-infarct, or vascular, dementia results from a series of small strokes that progressively destroy the brain. Dementia can also be caused by Huntington diseasesyphilismultiple sclerosisacquired immune deficiency syndrome (AIDS), and some types of encephalitis. Treatable dementias occur in hypothyroidism, other metabolic diseases, and some malignant tumours. Treatment of the underlying disease in these cases may inhibit the progress of dementia.

Dementia is a condition characterized by the global impairment of intellectual capacity. Common early symptoms include personality changes, loss of interests, impairment of attention and concentration, difficulty with comprehension, and difficulty in handling abstract concepts. Later, increasing impairment of the capacity to retain new information, social withdrawal, unnecessary repetition of…
In addition to the mental symptoms that may accompany pellagra, other mental disorders more specifically related to the consumption of alcohol include mild dementia, which may persist for up to six months after cessation of alcohol ingestion, and a relatively uncommon chronic brain disorder called Marchiafava-Bignami disease, which involves the degeneration of the corpus callosum, the tissue…
By the early 21st century it Alzheimer’s was recognized as the most common form of dementia among older persons. An estimated 47.5 million people worldwide were living with dementia in 2016; that figure was expected to increase to 75.6 million by 2030.

There are three recognized stages of Alzheimer disease: preclinical, mild cognitive impairment (MCI), and Alzheimer dementia. For clinical diagnosis the two most relevant stages are MCI and dementia. Recognition of the preclinical stage acknowledges that the Alzheimer disease process begins before symptoms are apparent and anticipates advances in diagnostic testing that may eventually enable diagnosis at the preclinical stage.

MCI often is subdivided into different types, namely amnestic and nonamnestic. One of the first symptom’s marking the transition from normal aging to Alzheimer disease is forgetfulness. This transitional stage represents amnestic MCI and is characterized by noticeable dysfunction in memory with retention of normal cognitive ability in judgment, reasoning, and perception. In nonamnestic MCI, impairments in cognitive functions related to attention, perception, and languagepredominate over deficits in memory. However, as MCI progresses to Alzheimer disease, memory loss becomes more severe, and language, perceptual, and motor skills deteriorate. Mood becomes unstable, and the individual tends to become irritable and more sensitive to stress and may become intermittently angry, anxious, or depressed. Those changes mark the transition to Alzheimer dementia, which in its advanced stages is characterized by unresponsiveness and loss of mobility and control of body functions; death ensues after a disease course lasting from 2 to 20 years.

About 10 percent of those who develop the disease are younger than 60 years of age. These cases, referred to as early-onset familial Alzheimer disease, appear to result from an inherited genetic mutation. The majority of cases of Alzheimer disease, however, develop after age 60 (late-onset); they usually occur sporadically—in individuals with no family history of the disease—although a genetic factor has been identified that is thought to predispose some of these individuals to the disorder. Rosacea, a chronic inflammatory condition of the skin, is also associated with an increased risk of Alzheimer disease, particularly among individuals aged 60 or older.

Neuropathology

Neuritic plaques and neurofibrillary tangles

The presence of neuritic plaques and neurofibrillary tangles in the brain are used to diagnose Alzheimer disease in autopsy. Neuritic plaques—also called senile, dendritic, or amyloid plaques—consist of deteriorating neuronal material surrounding deposits of a sticky protein called amyloid beta (or beta-amyloid). This protein is derived from a larger molecule called amyloid precursor protein, which is a normal component of nerve cells. Neurofibrillary tangles are twisted protein fibres located within nerve cells. These fibres consist of a protein, called tau, that normally occurs in neurons. When incorrectly processed, tau molecules clump together and form tangles.

Both neuritic plaques and neurofibrillary tangles, which also may be found in smaller amounts in the brains of healthy elderly persons, are thought to interfere in some way with normal cellular functioning. However, it is not known whether the plaques and tangles are a cause or a consequence of the disease. Research in animals suggests that amyloid-beta plaques form naturally in the brain in response to infection, serving to entrap microorganisms. The idea that amyloid beta serves as a natural antibiotic implies that Alzheimer disease may be in some way linked to brain infection, plaque formation being either excessive in older individuals or abnormal in some other way.

Other features have been noted in the brains of many persons with Alzheimer disease. One of these features is a deficiency of the neurotransmitter acetylcholine; neurons containing acetylcholine play an important role in memory.

Hyperinsulinemia

Abnormal insulin signaling in the brain has been associated with Alzheimer disease. Under normal conditions, insulin binds to insulin receptors, which are expressed in great numbers on the membranes of neurons, to facilitate neuronal uptake of glucose, which the brain depends upon to carry out its many functions. However, neurons in the brains of patients with Alzheimer disease have very few, if any, insulin receptors and therefore are resistant to the actions of insulin. As a result of the inability of insulin to bind to the neurons, it accumulates in the blood serum, leading to a condition known as hyperinsulinemia (abnormally high serum levels of insulin). Hyperinsulinemia in the brain is suspected to stimulate inflammation that in turn stimulates the formation of neuritic plaques. Abnormal insulin signaling in the brain has also been associated with nerve cell dysfunction and death, decreased levels of acetylcholine, and decreased levels of transthyretin, a protein that normally binds to and transports amyloid-beta proteins out of the brain.

Genetic variants

Underlying genetic defects have been identified for both late- and early-onset cases of Alzheimer disease. The identification and characterization of these defects has provided important insight into the pathology of Alzheimer disease and has informed the development of new approaches to diagnosis and treatment.

A defect in a gene known as APP, which codes for amyloid precursorprotein, may increase the production or deposition of amyloid beta, which forms the core of neuritic plaques. This gene, however, is responsible for only a very small percentage of all early-onset cases of the disease.

A defect in the gene that directs production of apolipoprotein E (ApoE), which is involved in cholesterol transport, may be a factor in the majority of late-onset Alzheimer cases. There are three forms of this gene—APOE2APOE3, and APOE4—two of which, APOE3 and APOE4, are associated with an increased risk of disease and influence the age of onset of disease.

Studies employing functional magnetic resonance imaging (fMRI) have shown that individuals between ages 20 and 35 who carry the APOE4variant frequently have increased activity in the hippocampus of the brain. This region plays a central role in the formation and recall of memories and is involved in the production of emotions. Scientists suspect that in some APOE4 carriers hyperactivity of the hippocampus early in life leads to this region’s later dysfunction, which contributes to the development of Alzheimer disease. Brain imaging using fMRI in young APOE4 carriers may be useful for identifying those carriers at greatest risk of disease.

Genetic screening to determine the status of a gene known as TOMM40(translocase of outer mitochondrial membrane 40 homolog [yeast]) can be used to provide additional information about the risk of Alzheimer disease and to predict the age of onset. There are several forms of this gene, which differ in their length due to variations that influence the number of repeats of a specific base-pair segment within the gene sequence. In persons who have inherited variants of TOMM40, the occurrence of a long form of the gene, in conjunction with either APOE3or APOE4, correlates with onset of the disease before age 80. In contrast, short forms of TOMM40 were found to correlate with onset of the disease after age 80.

Several other genes have been implicated in Alzheimer disease. Examples include CD33, which encodes a cell surface protein of the same name; PICALM, which encodes a protein involved in endocytosis (the cellular uptake of substances); and CD2AP, which encodes a protein that interacts with the cell membrane and may have a role in endocytosis.

Early Detection

Improved detection and treatments for Alzheimer disease are areas of concentrated scientific investigation. Progress in early detection has been of special significance, underlying important changes in diagnostic guidelines for Alzheimer disease. The first guidelines, implemented in 1984, restricted clinical diagnosis to the final stage of dementia, generally with diagnosis confirmed on autopsy. However, in 2011, as a result of improvements in diagnostic methods and in scientists’ understanding of the pathophysiology of Alzheimer disease, new guidelines that accommodated diagnosis at three different stages of the disease (preclinical, MCI, and dementia) were developed, allowing for more rapid incorporation of new or experimental diagnostic technologies.

Early detection of Alzheimer disease is based largely on advances in diagnostic imaging, on the discovery of biomarkers (physiological changes specific to and indicative of a disease), and on the development of methods sensitive enough to measure those biomarkers. Several detection methods being developed for Alzheimer disease include blood tests to measure increased expression of a protein present in certain white blood cells and positron-emission tomography to detect increased levels of an enzyme in cerebrospinal fluid.

A test designed to analyze spinal fluid for certain biomarker signatures indicative of Alzheimer disease has shown promise in early detection of the disease. Fluid for the test is collected via lumbar puncture (spinal tap). The sensitivity of the test is such that it can identify persons who are affected by mild cognitive impairment and hence are at the greatest risk of later developing the disease, thereby providing time for intervention strategies to delay its onset.

Lifestyle Factors And Prevention

A number of lifestyle factors that benefit cardiovascular health are associated with decreased risk of dementia and Alzheimer disease. Examples of such factors include regular physical exercise, a healthy diet, and low stress. In contrast, in persons genetically predisposed to Alzheimer disease, diets high in fat and sugar are suspected to negatively affect the brain by facilitating the development of neuritic plaques.

Dietary substances such as vitamin Bcaffeine, and alcohol also have been implicated in reducing the risk of Alzheimer disease. For example, a clinical trial involving a small number of subjects found that vitamin B12can slow the rate of brain atrophy in some persons with MCI. This effect is attributed to the ability of vitamin B12 to control blood levels of an amino acid known as homocysteine. Unusually high levels of homocysteine have been associated with an increased risk for Alzheimer disease. In studies of Alzheimer mice, intake of caffeine at concentrations equivalent to five cups of coffee in humans resulted in decreased levels of amyloid-beta proteins in the brain and blood. The effects of caffeine were strongest in mice displaying mild cognitive impairment. The substance also was found to improve memory significantly in these animals. In persons aged 75 and older who have normal cognitive function, the consumption of moderate amounts of alcohol, defined as being between 8 and 14 drinks per week (one drink equals 0.5 ounce of 100 percent alcohol), has been shown to reduce the risk of dementia by nearly 40 percent. However, in persons in the transitional stage to Alzheimer disease, who have symptoms of MCI, alcohol consumption is linked to accelerated progression toward dementia.

Another factor associated with a decreased risk for Alzheimer disease is rheumatoid arthritis, a chronic inflammatory disease of the connective tissues of the body. A protein known as GM-CSF (granulocyte-macrophage colony-stimulating factor), which is present in arthritis patients, is believed to stimulate the production of immune cells that destroy the amyloid-beta proteins. In studies of mice affected by cognitive impairment mimicking Alzheimer disease in humans, treatment with GM-CSF reduced the burden of amyloid plaques in the brain and was associated with improved performance on memory and learning tests. A form of GM-CSF known as sargramostim, which is used in the treatment of patients with acute myelogenous leukemia, is being investigated as a form of treatment for persons with Alzheimer disease.

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