Functional Foods, Ageing and Degenerative Disease
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Diet and the prevention of degenerative disease. New functional foods for agerelated diseases. Diet and the control of osteoporosis. Phytoestrogens and the control of osteoporosis. Vitamin D fortification and bone health. Calcium citrate TCC and bone health. Diet functional foods and oral health.
Dietary lipids and immune function. Improving gut health in the elderly. Probiotics prebiotics and gut health. Antiangiogenic functional food degenerative disease. Synbiotics and colon cancer. These cookies allow you to explore OverDrive services and use our core features. Without these cookies, we can't provide services to you. These cookies allow us to monitor OverDrive's performance and reliability. They alert us when OverDrive services are not working as expected. Without these cookies, we won't know if you have any performance-related issues that we may be able to address.
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Diffuse plaques, in turn, do not show abnormal neurites, appear to be more amorphous, and contain few, if any, amyloid fibrils, in diffused form. Diffuse plaques are often found in the brain of individuals with Alzheimer's disease. They may represent an early stage in the development of neuritic plaques. In individuals suffering from Alzheimer's disease, the number of neurofibrillary tangles NFT in the affected brain areas is about six times greater than in an intellectually normal but severely affected person.
NFTs are found mainly in the hippocampus and cerebral cortex; they have not been found in the cerebellum and spine. The tangle itself is intracellular and mostly composed of paired helical filaments PHF which, as the name suggests, are helically twisted pairs of protein filaments. These proteins are abnormally phosphorylated forms of tau protein often associated with microtubules and form complexes with another protein, ubiquitin, which is normally used by the cell to mark proteins destined for degradation MORI et al. Although NFTs are invariably found in patients with Alzheimer's disease, they can be found at lower levels in cognitively normal individuals, as well as in the brains of patients suffering from other neurological disorders.
These plaques and tangles can be seen, but not the synapse loss and neuron death. The third neurological feature of Alzheimer's disease is amyloid angiopathy, or deposition of amyloid protein in the blood vessel walls of the meninges and cortex. Severity of deposition varies widely, and the same characteristic is sometimes found in the brains of normal older individuals. Alzheimer's disease has a hereditary form and a non-hereditary form. The inheritance pattern is consistent with the idea that defective aging is transmitted as an autosomal dominant. Therefore, individuals develop full Alzheimer's disease when they inherit only one copy of the aberrant gene.
The remainder of affected individuals has a milder, non-hereditary form, which tends to become more apparent in advanced age; its etiology is still unclear. Currently, there are four known genetic alterations responsible for hereditary Alzheimer's disease, listed in Table 6. Amyloid is a generic term that describes proteins with a structure of beta-pleated sheets. The amyloid proteins related to Alzheimer's disease are derived mainly from the APP Amyloid Precursor Protein , located on chromosome The APP protein gene is expressed ubiquitously in mammals, by both neural and non-neural cells.
It is highly preserved in vertebrates and homologous proteins have been identified in the fruit fly Drosophila melalnogaster and roundworm Caerhabditis elegans. In all those cases, the protein encoded by APP is a transmembrane protein apparently involved in cell-cell signaling processes. Significant amounts of newly synthesized APP protein appear on the cell surface; some of these molecules may be cleaved at specific positions by unknown proteases.
Apparently, it is not the actual APP-encoded protein that causes Alzheimer's disease, but the derived fragments. All individuals affected by Down syndrome develop symptoms that are indistinguishable from those of Alzheimer's disease up to the age of 50, also presenting diffuse plaques as early as 12 years old. These observations were among the first evidence suggesting an important role played by the APP gene in the etiology of Alzheimer's disease.
Presenilin genes are located in chromosomes 1 and They encode two homologous transmembrane proteins that are also involved in cell-cell signaling. Dewji and Singer suggested that PS1 and PS2 presenilins 1 and 2 typically interact directly with the APP protein in an evolutionarily preserved intercellular signaling mechanism.
The ApoE4 gene plays a role in homozygous individuals for apolipoprotein E, ApoE4, who are more likely to develop Alzheimer's disease compared to individuals with ApoE3 or ApoE2 alleles. This may happen because the ApoE4 allele is not capable of binding to the microtubule tau protein, thus allowing free tau proteins to be hyperphosphorylated in an abnormal way, resulting in neurofibrillary tangles NFT characteristic of Alzheimer's disease. Inasmuch as it accumulates in its insoluble form plaque , this protein damages adjacent neurons directly, via neurotoxicity, or indirectly, via inflammatory reactions in microglial cells.
The mechanisms that produce such damage are becoming clearer. However, when bound to the receiver they generate an additional and sustained production of oxidants, resulting in oxidative stress and neurotoxicity YAN et al. In both cases, the resulting oxidative stress severely damages neurons and decreases their ability to withstand subsequent stresses. This reduction of oxidative resistance is probably exacerbated by low levels of mitochondrial activity, therefore low energy levels characteristic of patients with Alzheimer's disease DAVIS et al.
The low energy levels may be derived from mitochondrial damage induced by oxidative stress. Other metabolic changes probably include altered phosphorylation of tau protein and the formation of paired helical filaments PHF in neuritic plaques and neurofibrillary tangles NFT.
However, there is no strict relationship between level of damage and the extent of observed behavior changes. Education, culture and socioeconomic status enable a significant modulation of the result. If mental activity stimulates complex neural circuits, resulting redundancies may enable multiple additional routes through which information can enter and exit, and may mean that using the mind can prevent its loss. Recent research in Brazil and abroad seeks new alternatives and suggests new paths to attain, if not the cure, at least the most effective control of the development of Alzheimer's disease.
According to Tunes , FM-USP researchers identified phospholipase A2 enzyme in the blood, which they hope might be an effective biomarker for early detection of Alzheimer's disease or even the key to its cure. Wagner Farid Gattaz, one of the team leaders, examined the blood of healthy older individuals and compared it with samples of patients with Alzheimer's and mild cognitive impairment MCI , a disorder characterized merely by memory decline.
Both investigated groups AD and MCI showed decreased levels of phospholipase A2 PLA2 , an enzyme that acts on the metabolism of phospholipids, cell membrane components. The more impaired the brain functions, the lower the levels of phospholipase A2. It was found that, besides being produced by the pancreas as a digestive enzyme, this enzyme is present in all cells, including neuron cells.
The membrane of neurons is formed by a double layer of phospholipids. It was noted that phospholipase A2 was reduced in the brain, and that this decrease related to the intensity of brain injury; the lower the level of enzyme, the greater the occurrence of senile plaques. A link was discovered between reduced PLA2 in the brain and in the blood. The presence of PLA2 in the blood allows extrapolations to activity in the brain. A potential biomarker for Alzheimer's disease had been found. E4 is one of the three forms of the gene that encodes apolipoprotein E ApoE4 ; the other two genes encode the E2 and E3 alleles.
ApoE is a plasma protein related to transporting cholesterol to the liver, brain and other tissues. In blood testing for E4 allele, 20 control patients healthy older individuals , 41 patients with Alzheimer's and 21 with mild cognitive impairment MCI were analyzed.
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In this study, Bottino et al. At the UNESP campus in Araraquara, the team of pharmacist Vanderlan da Silva Bolzani extracted from Senna spectabilis , a tree up to 6m tall with green leaves and yellow-gold flowers, known as whitebark senna, a substance called spectaline, whose derivatives act against Alzheimer's. Three compounds derived from spectaline prevent the destruction of a substance responsible for communication between neurons and the neurotransmitter acetylcholine, associated with the formation of memory, thus increasing the amount of acetylcholine in the nervous system by inactivating acetylcholinesterase.
The advantage is that these compounds are not toxic like tacrine and rivastigmine, two of the drugs still used to fight damage caused by Alzheimer's. As they act on the acetylcholinesterase enzyme that degrades acetylcholine, spectaline and its derivatives may also aid in treating other neurological diseases, such as Parkinson's disease.
Taurine, essential for the absorption of fat by the intestine, acts in the nervous system like an antidote against the effects of the beta-amyloid peptide, which in very low amounts apparently stimulates the growth of neurons, but in Alzheimer's disease is produced uncontrollably, causing damage to thousands of nerve cells. Generated by the normal degradation of an important protein for the functioning of neurons, amyloid precursor protein APP , beta-amyloid peptide binds to other molecules equal to it, outside the cells. Near spherical aggregates, called oligomers, are initially formed, followed by long strands known as amyloid fibers.
In contact with the outer surface of nerve cells, beta-amyloid fibers bind with various proteins, one of them in particular, the glutamate receptor, associated with learning and memory formation. This large amount of positive particles alters for an extended period the electric charge inside the neurons, causing their death.
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Such protective action was also observed when replacing taurine with a drug used to combat epilepsy, phenobarbital, which has the disadvantage of causing dependence and undesirable effects, such as drowsiness and mental confusion. The UFRJ team showed that taurine is not the only alternative to offset the imbalance of electric charges generated by beta-amyloid. The hormone melatonin, responsible for the induction of sleep, released mainly at night by the pineal gland, also prevents the death of neurons by acting in a manner similar to taurine.
The team from UFRJ also demonstrated that two organic compounds, 2,4-dinitrophenol DNP and 3-nitrophenol, prevent neuron death by blocking the formation of beta-amyloid fibers or even by undoing them after they are formed. In the nervous system, two spectaline derivatives prevent the elimination of acetylcholine by inactivating acetylcholinesterase, consequently improving the ability to retain information without interacting with other substances of the central nervous system, a mechanism similar to that of another natural compound, galantamine, isolated from Galanthus nivalis , a plant up to 1m tall with white flowers, nowadays used in the treatment of Alzheimer's.
Functional Foods, Ageing and Degenerative Disease
In the rest of the body, the molecules of Senna spectabilis spectaline act as a potent analgesic. Most interestingly, in addition to improving the memory, spectaline derivatives are not toxic like tacrine, the drug most commonly used in the treatment of Alzheimer's. Recently, the Unesp team obtained the provisional patent registration of all spectaline derivatives in Brazil.
The teams are now working on the development of a drug based on spectaline derivatives that can be tested in humans. The aforementioned information was extracted from the report by Zorzetto The APP protein crosses the cell membrane, with most of it remaining outside the cell, while the rest is internal. Members of this set of proteases use aspartic acid to catalyze the lytic reaction of proteins.
Enzymes from the aspartic protease family that employ a pair of aspartic acid to activate the water molecule in the hydrolysis reaction. Its previously known three-dimensional structure was used as a guide for the computerized design of potentially inhibitory drugs. Until , these inhibitors were not ready for clinical trials.
The biggest challenge is to develop potent compounds small enough to penetrate the brain. Unlike blood vessels in other parts of the human body, brain capillaries are lined with very long endothelial cells. As there is little space between cells, protease inhibitors must be able to pass through the cell membrane to reach the posterior brain tissues, and most large molecules cannot overcome this blood-brain barrier. This second protease performs the rare feat of using water to hydrolyze the protein within the normally hydrophobic environment of the cell membrane.
However, a drug candidate developed by pharmaceutical company Eli Lilly has passed safety tests on volunteers. The compound is about to enter the next level of testing in patients with early Alzheimer's. Such molecules do not interact with aspartic acid; rather, they bind to another point of the enzyme and change its shape. One of these drugs, Flurizan, identified by a team from the University of California at San Diego and Mayo Clinic USA , has proven to be very promising in patients in the early stages of Alzheimer's and is already entering the stage of more advanced clinical trials in the United States, which will include more than 1, people.
One approach is active immunization, which involves recruiting the patient's own immune system to attack the protein. In mice there was improvement in learning and memory, which led to initial human trials. Follow-up research indicated that treatment may have caused inflammation by stimulating the T cells of the immune system, which are excessively aggressive to amyloid deposits.
Produced in guinea-pig cells and genetically engineered to prevent rejection in humans, these antibodies would hardly cause encephalitis, as they would not trigger a damaging T-cell response in the brain. A passive immunization treatment developed by Elan Corporation has already made progress with clinical trials in humans.
Although passive immunization appears to be more promising at the moment, active immunization has not yet been ruled out. Some compounds interact directly with the protein to keep it dissolved in the fluid outside the brain neurons, preventing the formation of noxious clusters. The Alzhemed compound showed little or no toxicity even at high dosages, and treatment led to some cognitive improvement in patients with moderate Alzheimer's.
Phase 3 clinical trials for this drug are well under way. The other half, filaments of tau, a protein that causes neural tangles, is considered a promising target to prevent degeneration of brain neurons. Researchers are focusing on finding inhibitors capable of blocking kinases that fix an excessive amount of phosphates in the tau protein, which is an essential step for the activity of the secretases responsible for the formation of tangles. An exciting recent breakthrough involves cell therapy.
Mark Tuszynski and colleagues at the University of California in San Diego conducted skin biopsies of patients with mild Alzheimer's and inserted in the skin the encoding gene for neural growth factor NGF. The genetically engineered cells were then surgically introduced into the brains of those patients. The idea was for them to produce and secrete NGF, which would compensate for the loss of acetylcholine-producing neurons and improve memory.
Cell-based therapy was a clever strategy to distribute NGF, a high-molecular-weight protein, which would not otherwise be able to penetrate the brain. The results were good enough to warrant additional clinical trials. While some of these potential therapies have not paid off, scientists hope to find at least one agent that can effectively slow down or interrupt the gradual loss of neurons in the brain, a breakthrough that would save millions of people from the inexorable decline caused by Alzheimer's disease and pave the way for drugs to regenerate lost mental functions.
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The speed surprised American researchers, who used a special microscope multiphoton capable of monitoring in real time the deposition of amyloid plaques in live mice. There are people who die with Alzheimer's disease symptoms and do not have plaques in the brain, and many have plaques in the brain but do not develop the disease. At normal levels, the protein induces the brain to recruit protective substances.
One of the possibilities is the amino acid taurine, which exists in high levels in the young brain. According to Ferreira, taurine acts as an antidote to N-methyl-D-aspartic activation. Researchers have detected gene activity in the brain that produces higher than expected brain-derived neurotrophic factor BDNF compared to other parts of the brain. The findings favor the idea that protein loss is linked to the onset of Alzheimer's.
Izquierdo proved that injecting the brain-derived neurotrophic factor BDNF in the hippocampus is sufficient to restore to rats memory they had lost due to a deficiency in protein production. In addition, this factor promotes the growth of communication points between neurons synapses. At high doses it can give rise to tumors. There are substances in the brain that protect cells and others that attack them. Researchers understand that as much as they discover the biochemical pathways, disrupting them can have adverse and serious effects.
Researchers from different areas seem to agree on one point: in order to balance the biochemical pathways, the safest answer seems not to be in drugs that alter proteins levels, but in diet. Calorie restriction, the only procedure that science has ever proven to prolong the life of laboratory animals, seems to shut down genes which trigger inflammatory processes.
It also increases the levels of neurotrophic factor and WNT protein activity. When testing the effects of calorie restriction in rats aged 4 and 24 months, during one month, alternating periods of 24h fasting and 24h ad libitum, the following was observed: in the younger mice, corresponding to adult humans aged about 30 years, calorie restriction reduced experimentally-induced inflammation in the hippocampus and increased the concentration of brain-derived neurotrophic factor BDNF , a protein that protects neurons and promotes memory formation. Calorie restriction in older rats that did not diet when young causes oxidative stress, which along with inflammatory processes ends up causing brain cell death.
Perhaps restriction should be constant throughout life, or a calorie restriction level suitable for advanced ages must be found.
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Strict diets impose physiological stress that may be excessive in old age. In young people, in turn, stress can strengthen the body. For example, it seems to be useless to begin a diet to avoid brain degeneration in middle age. In an increasing aging population, it is essential to take care of health from the origin of life. According to the researchers, Alzheimer's begins in the brainstem, more specifically in an area called the dorsal raphe nucleus Figure 5 , and not in the cortex, which is the center of information processing and memory storage, as medicine traditionally postulates.
This idea is defended by Brazilian scientists in partnership with colleagues from three German universities. The researchers identified lesions in the dorsal raphe nucleus in eight older individuals who had no tangles in any other part of the brain.
Functional Foods The Silver Lining In Ageing
While all 80 individuals already had at least one tangle in the entorhinal cortex a region traditionally considered the first to be affected by Alzheimer's. Responsible for connecting the cortex to the spinal cord, the stem is not strictly part of the brain, but of the encephalon, which comprises brain, cerebellum and stem. Not everyone who forgets things, whether older or not, necessarily has Alzheimer's disease or some other type of dementia. Seeking the cure for Alzheimer's disease is an extremely noble ambition for medical research.
However, in the short term it may be more realistic to think of ways to slow down the progress of brain injuries leading to Alzheimer's and prevent as much as possible the appearance of cognitive problems that gradually reduce the quality of life of patients. Another multifunctional substance under study is bradykinin, a natural peptide with vasodilation action, thus an adjuvant in antihypertensive action. Bradykinin is found in the blood and other body tissues and released in higher levels in inflammation.
Discovered around the mid th century by Brazilian researchers, it now draws renewed attention for effects heretofore unimagined. Studies carried out in recent years have shown that bradykinin induces stem cells to transform into neurons and protects them from death in brain lesions. In adipose tissue, another line of work suggests that it regulates the release of the hormone leptin, which induces satiety and reduces fat accumulation. The hypothesis that bradykinin could have effects beyond lowering blood pressure and controlling localized inflammation, the body's natural response to injury, arose in the mids with research by the biochemist Alexander Henning Ulrich at the University of Hamburg, Germany.
Ulrich investigated the mechanisms of proliferation of neural tissue tumors and observed that bradykinin triggered certain signaling mechanisms in these cells. He found that when binding to the B2 receptor on the surface of the stem cell, bradykinin triggers a chain of chemical reactions that modify the intracellular environment.
These ions function as a code that activates certain groups of genes in the nucleus and defines the fate of the stem cell: to continue multiplying and preserve its potential to originate different cell types, or to specialize in a certain function. The researchers observed that in the natural process of differentiation, the number of bradykinin receptors increases gradually.
In addition, cells release to the external environment part of the bradykinin they manufacture, influencing the functioning of their neighbors. This results in the emergence of neurons sensitive to the neurotransmitter acetylcholine, a chemical messenger that carries information from one brain cell to another, as detailed by Martins et al. According to the researchers, bradykinin does not initiate cell differentiation, but defines the pathways that cells will follow.
Neuron production was even greater when a compound called captopril was added to the stem cells in differentiation. This is the first antihypertensive drug to indirectly act in the preservation of bradykinin, keeping it active longer, through the inhibition of the enzyme that converts angiotensin I into angiotensin II ACE , by captopril. A greater production of neurons may be interesting in some situations. Experiments with animals have shown that neuronal replacement was not the only beneficial effect of bradykinin on the central nervous system.
Recent tests indicate that bradykinin can prevent the death of neurons in ischemia, an interruption of oxygen and nutrient flow caused by clogged blood vessels. Rats were treated with N-methyl-D-aspartic in the brain region that reproduces damage by ischemia. This compound, better known as NMDA, causes a torrent of calcium to enter the cells at 1, times the normal rate, killing them. Direct action of bradykinin on energy metabolism was identified when a type of transgenic mouse fattened less than common mice.
The difference between the two groups of rodents is that the transgenic animals did not have in their cells the B1 receptor, to which a byproduct of bradykinin binds and triggers phenomena typical of inflammation. Animals without the B1 receptor were more sensitive to the hormone leptin, according to Mori et al. This hormone induces satiety and increases the body's energy consumption. Elimination of B1 receptor apparently induces cells to produce more B2 receptor, to which bradykinin binds, suggesting that it regulates sensitivity to leptin.
Although the synthetic form of bradykinin has existed for almost half a century, it has not been approved for use in humans for having caused, in some studies, serious undesirable effects such as significant cerebral edema and low blood pressure. The hope of the researchers is to obtain an analogous molecule of bradykinin that causes fewer side effects and is also neuroprotective.
A few atypical cases have been reported in recent years. Samples of those brains donated to the USP-SP encephalon bank were analyzed under a microscope and revealed plaque clusters and protein tangles, hallmarks of the advanced stages of Alzheimer's disease. The researchers could not understand at the time why those people did not develop dementia.
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In dementia there is a drastic reduction of neurons in the hippocampus and cortex, the brain regions responsible for memory consolidation and reasoning. On average, one in 10 people over the age of 65 has the clinical signs of Alzheimer's. The disease first manifests itself with small slips of memory, which over time become more frequent, followed by failure in moral judgment, in perception of space and time, and increased difficulty in communicating.
Average survival time is eight years, during which the symptoms worsen until total incapacitation. It has been known for quite some time that dementia is caused by the destruction of synapses, the trillions of connections between the 86 billion neurons, the brain cells that store and transmit information from which memories and thoughts emerge. A healthy neuron receives up to 10, synapses from other neurons, exchanging electrical signals and substances that keep it alive. In Alzheimer's, neurons prevented from maintaining synapses atrophy and die.
As a consequence, hippocampal volume and cortex thickness decrease, which can be seen in magnetic resonance imaging MRI. In partnership with neurologist Fernando Cendes, also from Unicamp, researchers have been perfecting a new way of early identification of Alzheimer's disease: the use of neuroimaging to evaluate brain activity, and not just anatomy.
The technique is to observe brain activity in functional magnetic resonance imaging fMRI , when patients are relaxed, not thinking of anything. Even when people are resting, some areas of the brain are activated simultaneously, pulsating at the same frequency, which suggests that groups of neurons are communicating. The researchers also observed a relationship between network connection failures and degree of memory loss. According to Balthazar et al. Autopsy of brain tissue reveals an excess of so-called neuritic plaques, anchored in ramifications of neurons and neurofibrillary tangles within the atrophied neurons.
These signs are especially found in the hippocampus and in the cerebral cortex. Until a few years ago, most researchers believed that neuritic plaques were responsible for synaptic dysfunctions. Usually produced by the brain, this protein is deformed in Alzheimer's disease. Further research suggests that these oligomers also form the neurofibrillary tangles which prevent the transport of substances within neurons and contribute to their death.
According to this line of reasoning, plaque formation would be an attempt by the organism to remove the oligomers from the cells and away from the synapses. The discovery of asymptomatic Alzheimer's disease patients reinforced this hypothesis.
The first descriptions of such cases came from studies in the United States that monitored hundreds of older people. Asymptomatic individuals must possess some unknown physiological mechanism that protects their neuron networks from the effects of oligomers, something that removes the oligomers from the synapses by rapidly aggregating them into plaques. One factor to explain this mechanism is the more efficient performance of insulin in the brain of asymptomatic patients. Unlike what occurs in other organs, the role of insulin in the brain seems not to be control of glucose metabolism, but memory consolidation and formation of new synapses.
In this work the authors presented new neuronal mechanisms that cause loss of synapses in mice and monkeys similar to Alzheimer's. The study also showed that a drug used to treat type 2 diabetes liraglutide blocked neuronal damage in Alzheimer's animal models. Currently, a team from Imperial College London is testing liraglutide in people with Alzheimer's.
Another hypothesis is that asymptomatic patients have a greater cognitive reserve, perhaps resulting from a more complex synapsis network compared to individuals who develop dementia. This reserve would be more resistant to the effects of oligomers. This idea comes from the observation that asymptomatic patients are usually people with a higher level of education or who learned to speak and write early in childhood.
At Unicamp, Balthazar is attempting to confirm the protective effect of the cognitive reserve by comparing the connectivity of neural networks in older patients with different levels of education, reading habits and social life. Polo-Hernandez et al. In addition to this function, oleic acid promotes the formation of synapses by stimulating the expression of pre- and post-synaptic proteins and their approximation.
That confirms the role of oleic acid in postnatal brain development as an important factor in bidirectional astrocyte-neuron communication, enabling the formation of the final network that makes up the nervous tissue. Hamilton et al. The authors demonstrated that interference in the signaling or synthesis of oleic acid blocked the proliferation of neural stem cells NSC in mouse models for AD. In the brain postmortem of patients with AD and triple transgenic mouse models for AD 3xTg-AD they found an accumulation of neutral lipids in ependymal cells, the main support cells in the frontal brain for brain stem cells.
Mass spectrometry and micro-array analyses identified triglyceride deposits enriched with metabolized oleic acid at this specific focus, unrelated to a defect in peripheral metabolism. In wild-type mice they observed that a localized increase of oleic acid was sufficient to reproduce the accumulation of triglyceride on ependymal cells and to inhibit the proliferation of NSCs. The study supports a pathogenic mechanism by which the disorder of the localized lipid metabolism, due to AD, inhibits homeostasis and normal neural stem cell NSC function.
Animal models have been used to study pathogenesis in degenerative diseases, but no particular model has been able to reveal all pathological changes in patients with AD. Therefore, extensive validation of therapeutic targets in different models will be indispensable before clinical research can advance.
Functional foods, ageing and degenerative disease 
In recent research, Huang et al. These same animals also showed improved performance in memory tests. The authors suggest that this type of study should be repeated in other animal models, since it represents a noninvasive form with therapeutic potential for AD. The structures of the multipotent anti-DA agents are diverse, yet they are all polyphenols. Data from the literature accumulated to date show that several anti-AD agents have been identified from foods, with most showing pharmacological effects.
However, it should be borne in mind that the anti-Alzheimer potential identified in vitro is not necessarily reproduced in vivo , because factors such as bioavailability and interactivity may influence the behavior of these agents. Sakamoto et al. DHA, polyunsaturated omega-3 fatty acid, is an essential component for the formation of phosphatides in membranes and has been recognized as essential in cognitive functions. Low levels of DHA in the blood or brain have been associated with various neurocognitive disorders, including Alzheimer's disease, in animal models.