alzheimers causes

Brain changes linked with Alzheimer's years before symptoms appear

  • A long-running study found subtle cognitive deficits evident 11-15 years before clear impairment, as were changes in tau protein.

A very long-running study involving 290 people at risk of Alzheimer's has found that, in those 81 people who developed MCI or dementia, subtle changes in cognitive test scores were evident 11 to 15 years before the onset of clear cognitive impairment. They also showed increases in the rate of change of tau protein in cerebrospinal fluid an average of 34.4 years (for t-tau, or total Tau) and 13 years (for a modified version called p-tau) before the beginning of cognitive impairment.

https://www.eurekalert.org/pub_releases/2019-05/jhm-bcl051419.php

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Blood-clotting protein implicated in cognitive decline and Alzheimer's

  • A blood-clotting protein called fibrinogen has been shown to provoke the brain's immune cells into destroying synapses. The process begins with fibrinogen leaking from the blood into the brain.
  • Another study has found that nearly half of all dementias begin with a breakdown of the gatekeeper cells (pericytes) that help keep fibrinogen out of the brain.

Alzheimer's disease is associated with abnormalities in the vast network of blood vessels in the brain, but it hasn’t been known how this affects cognition. A study has now shown that a blood-clotting protein called fibrinogen plays a part.

The study found that fibrinogen, after leaking from the blood into the brain, activates the brain's immune cells and triggers them to destroy synapses, which are critical for neuronal communication.

Loss of synapses is known to cause memory loss, and the study found that preventing fibrinogen from activating the brain's immune cells protected Alzheimer's mice from memory loss.

Moreover, fibrinogen had this effect even in brains that lack amyloid plaques.

The findings help explain how elderly people with vascular pathology could show similar rates of cognitive decline as age-matched people with amyloid pathology. The same human studies also found that those with both types of pathology had much worse and more rapid cognitive decline.

Another study suggests that nearly half of all dementias, including Alzheimer's, begins with the breakdown of the smallest blood vessels in the brain and the "gatekeeper cells" that surround and protect the capilleries.

The collapse of pericytes (the gatekeeper cells) reduces myelin and white matter structure in the brain. They do this via fibrinogen. Fibrinogen develops blood clots so wounds can heal but when the gatekeeper cells fail, too much fibrinogen enters the brain and causes white matter to die.

Mouse studies showed that controlling fibrinogen levels can reverse or slow white matter disease.

Postmortem study of human brains found that Alzheimer’s brains had about 50% fewer gatekeeper cells and three times more fibrinogen proteins in watershed white matter areas, compared to healthy brains.

The mouse study found that white matter changes in mice began as early as 12 to 16 weeks old, the equivalent of 40 years in humans.

When an enzyme known to reduce fibrinogen was introduced into the mice, white matter volume returned to 90% of their normal state, and white matter connections were back to 80% productivity.

https://www.eurekalert.org/pub_releases/2019-02/gi-anc020519.php

https://www.eurekalert.org/pub_releases/2018-02/uosc-hoa020218.php

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Brain blood flow deficits in Alzheimer's explained

  • Blood flow deficits in the brain, seen early on in Alzheimer's, have now been linked to some capilleries being block by white blood cells.

It’s been known that decreased blood flow in the brain occurs in people with Alzheimer's, and recent studies suggest that brain blood flow deficits are one of the earliest detectable symptoms of dementia. A study has now shown why it occurs: a small percentage of capillaries, the smallest blood vessels in the brain, are blocked by white blood cells stuck to the inside of the capillaries.

Recent research has shown that capilleries are vital for monitoring and directing blood flow around the brain.

https://www.eurekalert.org/pub_releases/2019-02/cu-rct021119.php

https://www.nature.com/articles/s41593-018-0329-4

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How blood flow is controlled in the brain

  • A study shows that blood is stored in the blood vessels in the space between the brain and skull, and its flow  is closely linked to the flow of cerebrospinal fluid in and out of the brain's ventricles.
  • A second study shows that capilleries, the smallest blood vessels in the brain, monitor the flow of blood within the brain and actively direct it to the areas that need it the most.

Increases in brain activity are matched by increases in blood flow. Neurons require a huge amount of energy, but can’t store it themselves, so must rely on blood to deliver the nutrients they need.

Two new studies help explain how blood flow is controlled.

The first study found blood appears to be stored in the blood vessels in the space between the brain and skull.

When the heart pumps blood into cranium, only a fraction of it flows into the capillaries that infuse the brain. The arteries in the cranium expand to store the excess blood. This expansion pushes out cerebrospinal fluid into the spinal column. When the heart relaxes, the drop in the pressure pushing blood through the arteries causes them to contract and the blood is pushed into the brain's capillaries. This in turn forces used blood out of the brain into the veins between it and the skull. These cerebral veins expand to store this blood as it leaves the brain.

Crucially, the study shows that the flow of blood in the veins leading out of the cranium is closely linked to the flow of cerebrospinal fluid in and out of the brain's ventricles.

The second study looked at what happens further down the track.

It had been thought that capillaries were passive tubes and the arterioles were the source of action — but the area covered by capillaries vastly surpasses the area covered by arterioles. So new findings make sense: that capillaries actively control blood flow by acting like a series of wires, transmitting electrical signals to direct blood to the areas that need it most.

To do this, capillaries rely on a protein (an ion channel) that detects increases in potassium during neuronal activity. Increased activity of this channel facilitates the flow of ions across the capillary membrane, thereby creating a small electrical current that communicates the need for additional blood flow to the arterioles, resulting in increased blood flow to the capillaries.

If the potassium level is too high, however, this mechanism can be disabled. This may be involved in a broad range of brain disorders.

https://www.eurekalert.org/pub_releases/2017-05/lbu-ffi050217.php

https://www.eurekalert.org/pub_releases/2017-03/lcom-ei032417.php

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New mechanism adds to understanding of Alzheimer's causes

  • Age-related changes in gene enhancers have been linked to faster cognitive decline in Alzheimer's brains.

New findings identify a mechanism that accelerates aging in the brain and gives rise to Alzheimer's disease.

The findings center on “enhancers”, which turn the activity of genes up or down based on influences like aging and environmental factors. Comparing enhancers in brain cells of people at varying stages of Alzheimer's and healthy people has revealed that in normal aging, there is a progressive loss of important epigenetic marks on enhancers. This loss is accelerated in the brains of people with Alzheimer's.

These enhancers also over-activate a suite of genes involved in Alzheimer's pathology, spurring the formation of plaques and tangles, and reactivating the cell cycle in fully formed cells — a highly toxic combination.

The study also links enhancer changes to the rate of cognitive decline in Alzheimer's patients.

https://www.eurekalert.org/pub_releases/2019-05/vari-rtc051719.php

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Impaired waste management in the brain a cause of Alzheimer's?

  • A mouse study has shown that, as cells age, their ability to remove damaged proteins and structures (autophagy) declines, due to a decrease in the cell components (autophagosomes) that collect the damaged proteins.
  • A study found that the process of breaking down defective mitochondria and recycling the components (mitophagy) is impaired in those with Alzheimer's.
  • Microglia clear damage by engulfing the damaged matter then releasing it inside exosomes, which can be absorbed by other cells. Studies have now shown that these exosomes, designed to transmit information, can also spread harmful tau & amyloid-beta protein.
  • A mouse study has shown how amyloid plaques lead to tau tangles, and that weakened microglia facilitate this. It also links weak microglia to the risky variant of the TREM2 gene.
  • However, the common TREM2 variant is linked to faster plaque growth at later stages.
  • TREM2 appears to modify the way immune cells respond to tau tangles.
  • Another mouse study found that overactive microglia (achieved by turning off another gene) were linked to both better removal of amyloid-beta, and loss of synapses. This may help explain why reducing amyloid plaques often fails to improve cognition.

Aging linked to impaired garbage collection in the brain

A mouse study has shown that, as cells age, their ability to remove damaged proteins and structures declines.

The process of waste management, called autophagy, involves a component within the cell (an autophagosome) engulfing misfolded proteins or damaged structures (putting them in a garbage bag, essentially). The autophagosome then fuses with a second cellular structure, called a lysosome, that contains the enzymes needed to breakdown the garbage, allowing the components to be recycled and reused.

It’s thought that this decline in autophagy makes neurons more vulnerable to genetic or environmental risks.

The mouse study found that aging brought a significant decrease in the number of autophagosomes produced, along with pronounced defects in their structure.

However, activating the protein WIPI2B restored autophagosome formation.

https://www.eurekalert.org/pub_releases/2019-07/uops-tot071919.php

Breakdown in cleaning process in mitochondria linked to Alzheimer's

A cleaning process in brain cells called mitophagy breaks down defective mitochondria and reuses the proteins that they consist of. When the process breaks down, defective mitochondria accumulate in brain cells.

Research has now found that this is markedly present in cells from both humans and animals with Alzheimer's. Moreover, when active substances targeted at the cleaning process were tried in live animals, their Alzheimer's symptoms almost disappeared.

https://www.eurekalert.org/pub_releases/2019-02/uoct-oc021419.php

Microglia may spread toxic tau during early Alzheimer's

A 2015 study found how toxic tau fibrils spread during the early stages of Alzheimer's disease. Apparently the fibrils (accumulations of tau proteins) can be carried from one neuron to another by microglia.

Microglia act as the brain's immune cells, in which role they identify and clear damage and infection. They clear damage by first engulfing dead cells, debris, inactive synapses or even unhealthy neurons, then releasing nano-scale particles called exosomes, which can be absorbed by other cells.

It used to be thought that exosomes simply help the cell to get rid of waste products. It now appears that cells throughout the body use exosomes to transmit information. This requires them to contain both proteins and genetic material, which other cells can absorb. Hence their ability to spread tau protein, and hence, it now seems, their ability to also transport amyloid-beta.

http://www.eurekalert.org/pub_releases/2015-10/bumc-rdr100515.php

https://www.eurekalert.org/pub_releases/2018-06/lu-nmb061318.php

Microglia link Alzheimer’s amyloid and tau

Amyloid plaques and tau tangles are key biomarkers for Alzheimer’s, but research indicates that it is the tau tangles that are the real problem — the main problem with amyloid plaques is that they lead to tau tangles. A new study indicates how that happens.

A mouse study modified the TREM2 genes, which affect the health of microglia. So some mice carried the common variant of the gene, meaning that their microglia were fully functional, and some carried the risky variant, or no gene at all.

When seeded with tau protein from Alzheimer’s patients, those brains with weakened microglia produced more tau tangle-like structures near the amyloid plaques than in mice with functional microglia.

It was also revealed that microglia normally form a cap over amyloid plaques that limits their toxicity to nearby neurons. When the microglia failed to do that, neurons suffered more damage, creating an environment that fostered the formation of tau tangle-like lesions.

The findings were supported by the finding that humans with TREM2 mutations who died with Alzheimer’s had more tau tangle-like structures near their amyloid plaques than people who died with Alzheimer’s but didn’t have the risky gene.

https://www.futurity.org/alzheimers-disease-amyloid-plaques-tau-2095692/

https://www.eurekalert.org/pub_releases/2019-06/wuso-aml062319.php

However, it should be noted that in more advanced stages of Alzheimer’s, mice with the common TREM2 variant showed faster plaque growth. This appears to be linked to the gene inducing microglia to produce ApoE, which enhances aggregate formation.

The finding adds to evidence that Alzheimer's treatment has to take into account the stage at which the disease is at.

https://www.eurekalert.org/pub_releases/2019-01/d-gc-dic010819.php

Another study that modified the TREM2 gene in mice found that the difference between those with the gene and those without was not in the amount of tau tangles, but rather in the way their immune cells responded to the tau tangles. The microglia in mice with TREM2 were active, releasing compounds that in some circumstances help fight disease, but in this case primarily injured and killed nearby neurons. The microglia in mice without TREM2 were much less active, and their neurons were relatively spared.

https://www.eurekalert.org/pub_releases/2017-10/wuso-agp100617.php

http://www.futurity.org/trem2-alzheimers-disease-1573272/

Overactive microglia have multiple effects

A study found that, if the gene for the TDP-43 protein was turned off in microglia, its activity increased, and amyloid-beta was removed very efficiently. However, when TDP-43 was switched off in microglia in mice, it didn’t just get better at removing amyloid-beta, but also led to a significant loss of synapses.

Clearly, dysfunction of microglia is a complicated business, and it’s suggested that such dysfunction may be one reason why many Alzheimer's medications reduce amyloid plaques but fail to improve cognition.

https://www.eurekalert.org/pub_releases/2017-06/uoz-osc062917.php

Classifying brain microglia

Microglia come in many forms. A survey of brain microglia has classified microglia into at least nine distinct groups, including some types never detected in the past. Some types appeared almost exclusively in the embryonic or newborn stages, others only after injury.

One group tended to cluster near the brain's developing white matter. Another appears to be very inflammatory compared with other microglia, and has been found in people with MS.

Microglia were most diverse early in brain development, in the aged brain and in disease.

https://www.eurekalert.org/pub_releases/2018-12/bch-cbm120518.php

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[4447] Stavoe, A. K. H., Gopal P. P., Gubas A., Tooze S. A., & Holzbaur E. L. F.
(2019).  Expression of WIPI2B counteracts age-related decline in autophagosome biogenesis in neurons.
(Dikic, I., Marder E., & Hurley J. H., Ed.).eLife. 8, e44219.

[4448] Fang, E. F., Hou Y., Palikaras K., Adriaanse B. A., Kerr J. S., Yang B., et al.
(2019).  Mitophagy inhibits amyloid-β and tau pathology and reverses cognitive deficits in models of Alzheimer’s disease.
Nature Neuroscience. 22(3), 401 - 412.

Maitrayee Sardar Sinha, Anna Ansell-Schultz, Livia Civitelli, Camilla Hildesjö, Max Larsson, Lars Lannfelt, Martin Ingelsson and Martin Hallbeck, Alzheimer disease pathology propagation by exosomes containing toxic amyloid-beta oligomers, Acta Neuropathologica, published online 13 June 2018, doi: 10.1007/s00401-018-1868-1 https://link.springer.com/article/10.1007/s00401-018-1868-1

[4451] Leyns, C. E. G., Gratuze M., Narasimhan S., Jain N., Koscal L. J., Jiang H., et al.
(2019).  TREM2 function impedes tau seeding in neuritic plaques.
Nature Neuroscience. 22(8), 1217 - 1222.

Parhizkar et al. (2019): "Loss of TREM2 function increases amyloid seeding but reduces plaque-associated ApoE", Nature Neuroscience, DOI: 10.1038/s41593-018-0296-9

Leyns C, Ulrich J, Finn M, Stewart F, Koscal L, Remolina Serrano J, Robinson G, Anderson E, Colonna M, Holtzman DM. TREM2 deficiency attenuates neuroinflammation and protects against neurodegeneration in a mouse model of tauopathy. Proceedings of the National Academy of Sciences. Week of Oct. 9, 2017.

[4452] Paolicelli, R. C., Jawaid A., Henstridge C. M., Valeri A., Merlini M., Robinson J. L., et al.
(2017).  TDP-43 Depletion in Microglia Promotes Amyloid Clearance but Also Induces Synapse Loss.
Neuron. 95(2), 297 - 308.e6.

[4464] Hammond, T. R., Dufort C., Dissing-Olesen L., Giera S., Young A., Wysoker A., et al.
(2019).  Single-Cell RNA Sequencing of Microglia throughout the Mouse Lifespan and in the Injured Brain Reveals Complex Cell-State Changes.
Immunity. 50(1), 253 - 271.e6.

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Researchers classify Alzheimer's patients in 6 subgroups

  • More evidence that Alzheimer's disease is not a single disease with a single cause and single pathway comes from a large study classifying patients into 6 groups, only two of which showed strong genetic association.
  • Another study using post-mortem brain tissue found that different genes were associated with different types of brain damage.

A study involving 4,050 people with late-onset Alzheimer's disease (mean age 80) has classified them into six groups based on their cognitive functioning at the time of diagnosis. A genetic study found two of the groups showed strong genetic associations.

The participants received cognitive scores in four domains: memory, executive functioning, language, and visuospatial functioning. The largest group (39%) had scores in all four domains that were fairly close to each other. The next largest group (27%) had memory scores substantially lower than their other scores. Smaller groups had language scores substantially lower than their other scores (13%), visuospatial functioning scores substantially lower than their other scores (12%), and executive functioning scores substantially lower than their other scores (3%). There were 6% who had two domains that were substantially lower than their other scores.

One group showed a very strong genetic association with 33 single nucleotide polymorphisms (SNPs) — this effect was stronger than the strongest effects found by an earlier and much larger international consortium study where Alzheimer's disease was treated as a single condition.

The memory group had a particularly strong relationship with the APOE e4 allele.

The participants were mostly white (92%) and 61% were female.

https://www.eurekalert.org/pub_releases/2018-12/uowh-rca120418.php

The finding is supported by another study using brain tissue from deceased patients with rare and common forms of Alzheimer’s, and from those who didn’t have the disease. The study showed that different genes are associated with different types of brain damage.

Those with the genes implicated in early-onset Alzheimer's (APP, PSEN1, and PSEN2) showed lower numbers of neurons and higher numbers of astrocytes than people who had Alzheimer’s but didn’t carry those mutations.

A similar pattern was found in patients with APOE4. However, carriers of TREM2 showed less neuronal loss and more damage to glial cells.

https://www.futurity.org/alzheimers-disease-genes-brain-cell-damage-1786192/

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Brain proteins involved in the development of Alzheimer's

  • When a particular fat molecule in the brain doesn't break down properly, cognition gets harder, and there's an increase in amyloid precursor proteins (which are part of the Alzheimer's cascade).
  • Tau proteins are also involved in the Alzheimer's cascade. A new study shows that individuals vary markedly in how quickly they spread in the brain.
  • A protein called SIRT6 has now been found to be crucially involved in DNA repair, to be severely deficient in those with Alzheimer's, and to be associated with learning impairment in mice.
  • A protein called NPTX2 may explain why some brains can cope with high levels of amyloid-beta much better than others.

Disrupted fat breakdown in the brain involved in Alzheimer’s?

The brain is rich in lipids (fats), which not only help insulate nerve fibers, but are also a crucial part of the membranes surrounding brain cells. One particular type that is highly enriched in the brain (sphingolipids) produces something called S1P. A mouse study has now found that when their brains were blocked from breaking down S1P, the mice began to show learning and memory problems. Moreover, there was a significant increase in the amount of APP (the precursor of amyloid-beta proteins, characteristic of Alzheimer’s) in their brains.

The problem is that S1P is broken down into simpler products, one of which is vital for autophagy — how cells digest and recycle their own components, when they don’t work properly. This finding suggests a new mechanism for the development of Alzheimer's and other dementias.

https://www.eurekalert.org/pub_releases/2017-05/uob-dfb051917.php

Spread of tau protein measured in Alzheimer's brains

A study involving 16 patients at different stages of Alzheimer's disease, who underwent memory tests and PET scans at 17-month intervals, has found a marked difference between individuals in how much tau protein is in the brain and how quickly it spreads. Moreover, there was a strong correlation between the amount of tau and how much episodic memory was impaired.

This may help explain why Alzheimer's progresses at such different rates between people.

https://www.eurekalert.org/pub_releases/2017-05/ki-sot051617.php

Low levels of protein SIRT6 implicated in Alzheimer's

It’s generally thought that aging is the result of DNA damage accumulation, because of the breakdown in DNA repair processes. A new mouse study has found that a crucial element in DNA repair is a protein called SIRT6. Mice deficient in SIRT6 showed marked learning impairments, and their brains showed more DNA damage, cell death, and hyperphosphorylated tau (a critical mark in several neurodegenerative diseases, as well as Alzheimer's).

Humans with Alzheimer's disease were also found to have a severe deficiency of the SIRT6 protein.

It’s suggested that SIRT6 loss, leading to DNA damage accumulation, may be the beginning of the chain that ends in Alzheimer’s and other neurodegenerative disease.

https://www.eurekalert.org/pub_releases/2017-05/aabu-bur050517.php

Low levels of 'memory protein' linked to cognitive decline in Alzheimer's disease

We know that high levels of amyloid-beta plaques are characteristic of Alzheimer's, but we also know that people can have high levels of amyloid without displaying symptoms of Alzheimer's. A new study shows that the reason for this apparent discrepancy may lie with another protein, called NPTX2.

It appears that memory loss occurs when high amyloid-beta occurs in combination with low levels of NPTX2.

The gene which expresses the protein NPTX2 belongs to a set of genes known as "immediate early genes," which are activated almost instantly in brain cells when an experience results in a new memory. The protein is used by neurons to strengthen the circuits that encode memories.

A study of 144 archived human brain tissue samples revealed that NPTX2 protein levels were reduced by as much as 90% in brain samples from people with Alzheimer's compared with age-matched brain samples without Alzheimer's. People with amyloid plaques who had never shown signs of Alzheimer's, on the other hand, had normal levels of NPTX2.

A mouse study then confirmed this link, by showing that cell function wasn’t affected by a lack of NPTX2 until a gene that increases amyloid generation was added. With both amyloid and no NPTX2, fast-spiking interneurons could not control brain "rhythms" which synchronize activity between neurons, thus creating circuits / networks that encode memories. Additionally, a glutamate receptor essential for interneuron function was also reduced — as it was in the human Alzheimer's brains.

A study of NPTX2 protein levels in the cerebrospinal fluid (CSF) of 60 living Alzheimer's patients and 72 controls found that

  • NPTX2 levels were 36-70% lower in people with Alzheimer's
  • lower cognitive scores were associated with lower levels of NPTX2
  • NPTX2 levels were more closely correlated with cognitive performance that tau proteins and amyloid-beta
  • NPTX2 correlated with the size of the hippocampus

https://www.eurekalert.org/pub_releases/2017-04/jhm-llo042417.php

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Alzheimer's disease consists of 3 distinct subtypes

  • A very small study points to three subtypes of Alzheimer's disease, each of which seems to be associated with:
    • different physiological abnormalities
    • different causes and risk factors
    • different symptoms / progression
    • different age-onsets.
  • This suggests that effective treatments need to be tailored to the subtype.

A two-year study which involved metabolic testing of 50 people, suggests that Alzheimer's disease consists of three distinct subtypes, each one of which may need to be treated differently. The finding may help explain why it has been so hard to find effective treatments for the disease.

The subtypes are:

  • Inflammatory, in which markers such as C-reactive protein and serum albumin to globulin ratios are increased.
  • Non-inflammatory, in which these markers are not increased but other metabolic abnormalities (such as insulin resistance, hypovitaminosis D, and hyper-homocysteinemia) are present. This tends to affect slightly older individuals than the first subtype: 80s rather than 70s.
  • Cortical, which affects relatively young individuals (typically 50s- early 70s) and appears more widely distributed across the brain than the other subtypes, showing widespread cortical atrophy rather than marked hippocampal atrophy. It typically presents with language and number difficulties first, rather than memory loss. Typically, there is an impaired ability to hold onto a train of thought. It is often misdiagnosed, typically affects people without a family history of Alzheimer's, who do not have an Alzheimer's-related gene, and is associated with a significant zinc deficiency (Zinc is implicated in multiple Alzheimer's-related metabolic processes, such as insulin resistance, chronic inflammation, ADAM10 proteolytic activity, and hormonal signaling. Zinc deficiency is relatively common, and associated with increasing age.).

The cortical subtype appears to be fundamentally a different condition than the other two.

I note a study I reported on last year, that found different molecular structures of amyloid-beta fibrils in the brains of Alzheimer's patients with different clinical histories and degrees of brain damage. That was a very small study, indicative only. However, I do wonder if there's any connection between these two findings. At the least, I think this approach a promising one.

The idea that there are different types of Alzheimer's disease is of course consistent with the research showing a variety of genetic risk factors, and an earlier study indicating at least two pathways to Alzheimer's.

It's also worth noting that the present study built on an earlier study, which showed that a program of lifestyle, exercise and diet changes designed to improve the body's metabolism reversed cognitive decline within 3-6 months in nine out of 10 patients with early Alzheimer's disease or its precursors. Note that this was a very small pilot program, and needs a proper clinical trial. Nevertheless, it is certainly very interesting.

http://www.eurekalert.org/pub_releases/2015-09/uoc--adc091615.php

Reference: 

Bredesen, D.E. 2015. Metabolic profiling distinguishes three subtypes of Alzheimer's disease. AGING, 7 (8), 595-600. Full text at http://www.impactaging.com/papers/v7/n8/full/100801.html

Bredesen, D.E. 2014. Reversal of cognitive decline: A novel therapeutic program. AGING, Vol 6, No 9 , pp 707-717. Full text at http://www.impactaging.com/papers/v6/n9/full/100690.html

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Inflamed iron-containing cells found in Alzheimer's brains

A post-mortem study of five Alzheimer's and five control brains has revealed the presence of iron-containing microglia in the subiculum of the Alzheimer's brains only. The subiculum lies within the hippocampus, a vital memory region affected early in Alzheimer's. None of the brains of those not diagnosed with Alzheimer's had the iron deposits or the microglia, in that brain region, while four of the five Alzheimer's brains contained the iron-containing microglia.

The microglia were mostly in an inflamed state. Growing evidence implicates brain inflammation in the development of Alzheimer's.

There was no consistent association between iron-laden microglia and amyloid plaques or tau in the same area.

Obviously, this is only a small study, and more research needs to be done to confirm the finding. However, this is consistent with previous findings of higher levels of iron in the hippocampi of Alzheimer's brain.

At the moment, we don't know how the iron gets into brain tissue, or why it accumulates in the subiculum. However, the researchers speculate that it may have something to do with micro-injury to small cerebral blood vessels.

This is an interesting finding that may lead to new treatment or prevention approaches if confirmed in further research.

http://www.eurekalert.org/pub_releases/2015-07/sumc-sss072015.php

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