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Alzheimer, feed forward cycle, neocortex, hippocampus and RNA quality

AD is a neurodegenerative disease of complex etiology (29, 30). The formation of neurofibrillary tangles (NFT), neuropil threads, and senile plaques have been implicated in the onset and development of the disease, but the relative causal weight of these and other factors in sporadic AD continues to be debated (30, 31). Although initiation and progression of AD may thus be multifactorial, it has been noted that incidence and regional distribution of NFT are most closely associated with the clinical manifestations of the disease (32, 33). NFT formation is the result of the accumulation of altered components of the neuronal cytoskeleton (34), and it has been suggested that “clogging” of neuronal processes and disruption of long-distance transport may underlie at least some of the cytopathological changes that characterize the disease (19).

We suggest that such cellular changes on one hand and deregulated expression and transport of dendritic RNAs on the other may be causally interrelated in AD. It has recently been speculated that non-protein-coding RNAs may be involved in AD (35), and we now show that expression of dendritic BC200 RNA, which is a translational repressor (3, 5), is differentially regulated in normal aging and in AD. In normal aging, BC200 levels in the neocortex decrease substantially after age 50. Because BC RNAs are prominently located throughout dendrites and at synapses (1, 2, 8), the substantial decline of BC levels may reflect the progressive atrophy of synaptodendritic structures that has previously been observed in normal aging (23, 36–39).

In AD, synapse loss and dendritic regression are substantial (40), but these degenerative changes are accompanied by significant dendritic sprouting and remodeling, often in the same neuron (30, 41, 42). Such reactive developments may be of a compensatory nature, directed at maintaining connectivity and plasticity. In one possible scenario, we therefore suggest that the substantially higher BC200 levels in AD, as compared with those in normal aging, may represent a molecular compensatory effort. If BC200 RNA is needed at the synapse for local translational control, its loss from synaptodendritic domains as the result of dendritic regression and clogging in AD may trigger compensatory mechanisms that result in the increased production of the RNA.

Increased synthesis of key synaptodendritic components may be an appropriate response in situations in which cargoes are not effectively delivered to postsynaptic sites. It may, at least initially or partially, be successful in overcoming moderate dendritic clogging that is caused by altered cytoskeletal components. Over time, however, such response may prove inadequate if further accumulation of cytoskeletal debris creates “roadblocks” that RNAs with dendritic destinations are no longer able to traverse. At this point, relative BC200 levels would begin to decrease in dendrites but increase in somata. In such cases, efforts to compensate would have failed because even increased production could no longer ensure that the RNA reaches its dendritic target sites. Transport deficits have previously been implicated in the progression of AD (18–20), and impaired microtubule-dependent transport, coupled with beginning axonal and dendritic blockage, may be an early event in AD that could eventually result in the local generation of amyloid-β peptides and thus in amyloid deposition (17).

Alternative scenarios are possible or even likely. Instead of, or in addition to, being reactive–compensatory to cytoskeletal degeneration, imbalances in the somatodendritic distribution of BC200 RNA could be causative because they may lead to aberrant local translational control. BC200 RNA contains a kink turn motif of the KT-58 subtype that has been implicated in dendritic transport of BC RNAs (9, 43). Because only slight perturbations of the kink turn motif architecture are sufficient to disrupt targeting (9), it is conceivable that single-nucleotide mutations in this region may prevent delivery of the RNA along the dendritic extent. Consequences would be twofold: compensatory elevation of BC200 transcription in an attempt to overcome dendritic delivery block and poor translational control in synaptodendritic domains. Consistent with this model, altered relative BC200 levels become manifest at a very early time point in the course of AD, possibly before clinical signs become detectable (44, 45).

A gradual worsening of somatodendritic BC200 imbalances may over time set off a self-reinforcing feed–forward cycle. Inadequate translational regulation in dendrites may lead to cytoskeletal overproduction and local dysfunction (16), which in turn would hinder the transport of mRNAs and protein synthetic machinery to postsynaptic target sites. In line with this concept, levels of somatodendritic RC3 mRNA have been shown to be significantly diminished in dendritic regions of AD brains (46). Having been disrupted in this manner, the system would find itself on a slow but accelerating course toward eventual catastrophe, manifesting as synaptic or plasticity failure (17, 30, 47–49). At the same time, increased perikaryal levels of BC200 RNA may inappropriately repress somatic protein synthesis and thus precipitate or exacerbate degenerative changes. We anticipate that future work, directed at the understanding of neuronal RNA transport and local translational control mechanisms, will be able to establish the respective contributions of the causative and reactive–compensatory scenarios.

The study samples come from the Adult Changes in Thought (ACT) study, a longitudinal research effort led by Eric B. Larson, M.D., M.P.H., and Paul K. Crane, M.D., M.P.H., of the Kaiser Permanente Washington Health Research Institute (KPWHRI) (formerly known as Group Health Research Institute) and the University of Washington School of Medicine to collect data on thousands of aging adults, including detailed information on their health histories and cognitive abilities.

“This collaboration with the Allen Institute for Brain Science has allowed us to gain insights never before possible into the relationships between neuropathology, gene expression, RNA quality, and clinical features tracked in the ACT study over more than 20 years,” says Larson, who has led the National Institute of Aging-supported study from its start in 1986 and is Vice President for Research and Health Care Innovation at Kaiser Permanente Washington.

Neural Networks: Sleep and memory – ScienceDirect

http://www.sciencedirect.com/science/article/pii/S0960982295001655

by TJ Sejnowski – ‎1995 – ‎Cited by 12 – ‎Related articles

During this generative sleep stage, the strengths of the feedforward synaptic … in the sense that only small changes are made during any one wake–sleep cycle. … sleep, the visual cortex is driven by brain-stem activity and the hippocampus …

Interaction between neocortical and hippocampal networks via slow …

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2180396/

by A SIROTA – ‎2005 – ‎Cited by 139 – ‎Related articles

This might be caused by the removal of tonic and phasic feed–forward … pool correlates with the duration of the oscillatory cycle, various brain rhythms can set …

Sleep and Brain Activity – Page 214 – Google Books Result

https://books.google.com/books?isbn=0123849950

Marcos G. Frank – 2012 – ‎Medical

So, to the degree that the hippocampal output during ripples originates in … in the prefrontal cortex and spreading through the whole neocortex and brain issue a … a feed forward manner favors the occurrence of another slow oscillation cycle …

Disorders of Brain, Behavior, and Cognition: The Neurocomputational …

https://books.google.com/books?isbn=0080862462

J.A. Reggia, ‎E. Ruppin, ‎D.L. Glanzman – 1999 – ‎Medical

… transmission in the piriform cortex, with a much weaker effect on feedforward … in the hippocampusgo much higher than ACh levels in neocortex (Marrosu et al., … rapid changes in modulatory dynamics within each cycle of the theta rhythm.

Microcircuits and their interactions in epilepsy: Is the focus out of focus?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4561622/

by JT Paz – ‎2015 – ‎Cited by 61 – ‎Related articles

1): 1) feed–forward inhibition, in which excitatory inputs from extrinsic brain regions recruit local inhibitory … Feed–forward inhibition in neocortex and hippocampus …. This cycle then repeats to propagate seizure activity to the next microcircuit.

Rhythms of the Brain – Page 374 – Google Books Result

https://books.google.com/books?isbn=019804125X

Gyorgy Buzsaki – 2006 – ‎Medical

Ahn SM, Freeman WJ (1974) Steady-state and limit cycle activity of mass of … of functionally segregated circuits linking basal ganglia and cortex. … Alger BE, Nicoll RA (1982) Feed–forward dendritic inhibition in rat hippocampal pyramidal cells …

Spatially segregated feedforward and feedback neurons support …

https://www.nature.com › nature neuroscience › articles

by FC Leitner – ‎2016 – ‎Cited by 13 – ‎Related articles

May 16, 2016 – The lateral entorhinal cortex (LEC) computes and transfers olfactory … Here we established LEC connectivity to upstream and downstream brain … RE⁺ neurons provide feedforwardprojections to the hippocampus while …… All animals were housed singly or in pairs and were kept on a 12 h light/dark cycle.

Dynamic Coordination in the Brain: From Neurons to Mind

https://books.google.com/books?isbn=0262014718

Christoph von der Malsburg, ‎William A. Phillips, ‎Wolf Singer – 2010 – ‎Medical

From Neurons to Mind Christoph von der Malsburg, William A. Phillips, Wolf Singer … and Transfer at theHippocampus–Entorhinal– Neocortical Interface György Buzsáki … the multisynaptic feedforward loops of the entorhi- nal–hippocampal system, … In each oscillatory cycle, recruitment of principal neurons is temporally …

Handbook of Brain Microcircuits – Page 166 – Google Books Result

https://books.google.com/books?isbn=0199780331

Gordon Shepherd, ‎Sten Grillner – 2010 – ‎Medical

(A) Multiple loops of the hippocampal-entorhinal (EC) circuits. … computation in successive layers of the EC-hippocampus (mainly) feedforward loop. … the main direction of information flow, withneocortical– hippocampal transfer taking place … Neurons that discharge within the time period of the gamma cycle (10–30 msec) …

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Connie’s comments:

The plaque, clogging , RNA quality and rhythm of the brain circuits are affected by quality of life, whole foods, sleep, stress, and affected by toxins in our environment.

Knowing the effects of the clogging and plaques in our brain from stress, lack of sleep, toxins and inflammation that started in our intestines and environment (pollution, carbon monoxide poisoning, metal toxicities, others) can help us prevent Alzheimer’s. The cure is prevention 20 years before our brain can no longer clean up the plaques and clogs.

For quality supplementation to reset your gene expression to a younger you, visit:

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Molecular cancer screen at a distance

Molecular biomarkers are independent of the presence of a detectable tumor mass or even the detection of intact transformed cells. Instead, they represent detection at a distance, using molecular signals in blood or excretia to indicate the presence of a cancer or pre-invasive lesion. These molecular biomarkers fall into four groups (Table 1).

Some are products of the neoplastic process that are shed by the tumors, such as mutated or hypermethylated DNA (‘carcinogenesis markers’). Others are molecular species generated by the host response to the cancer (‘response biomarkers’). Examples include antibodies, protein degradation products,¹² and acute phase reactants.¹³

A third group of biomarkers, like blood in stool or PSA in serum, are released in abnormal amounts as a result of the anatomical or metabolic disruption associated with a tumor (‘released biomarkers’).

The final group of molecular markers comprises factors associated with or supporting the underlying carcinogenesis (‘risk biomarkers’). Examples are high estradiol levels in relation to breast cancer or markers of human papilloma virus in relation to cervical cancer.

These classes of biomarkers will probably behave differently in early detection. Carcinogenesis markers are likely to be relatively specific for invasive or pre-invasive neoplasia, as they are essentially found only in on-going carcinogenesis.

Testing for PSA or blood in stool has already shown that released biomarkers can be non-specific: pathology other than cancer often leads to their release into blood and stool respectively.

Risk biomarkers are often abnormal in individuals without cancer; these are really risk factors, markers of cancer risk rather than markers of cancer itself.

Typically only a minority of individuals with the risk factors actually develop the associated disease.

Thus, just as benign masses can mimic tumors or obscure cancers in anatomical screening, pathological and metabolic processes will affect the specificity of molecular screening, especially if it is not based on carcinogenesis markers. PSA provides many examples: hemodilution of PSA levels in obese men,^{14, 15}distortion of levels by medication,¹⁴ and increases in levels from prostatitis.¹⁶ Inflammation – a risk factor for cancer in many organs — may be a particular problem as it shares molecular mediators with carcinogenesis.

One is that the tests are convenient and safe – typically requiring only the donation of blood, urine or stool. Measuring these molecular biomarkers does not involve tests that deliver radiation, a visit to the clinic, or unpleasant procedures as is needed for colonoscopy. Thus, the use of molecular biomarkers is likely to improve the uptake of screening by the general population and make repeated testing practical and affordable. This would increase the sensitivity of the screening process, and correspondingly increase the chances of detecting early cancers. However, it would also increase the potential for false positives, with the adverse downstream consequence of unnecessary diagnostic follow-ups.

Another advantage of molecular biomarkers is that they can easily be combined into panels using mathematical techniques such as logistic models or recursive partitioning to enhance sensitivity and specificity. Such combinations might be less susceptible to measurement artifacts than the individual markers. Also, the quantitative nature of many molecular markers means that they can potentially be personalized, using age, sex and race-specific norms, for example.

Pre-malignant lesions

Since the molecular defects of early cancer are often similar to those of intraepithelial neoplasia,⁴⁰molecular screening for cancers will likely identify substantial numbers of pre-invasive lesions. In organs such as the colorectum and cervix, these can be removed relatively easily to reduce risk of future cancer. Excision of pre-invasive lesions identified in less accessible tissues, such as the pancreas, entails considerable morbidity. It may not be clear what should be done to address the increased risk of invasive cancer, particularly as the natural history of these screen-detected lesions may not be well characterized.

Some risk biomarkers and some reaction biomarkers (such as antibodies) might remain in the abnormal range even after the responsible lesions are completely removed. For example, long-term hormonal patterns that promoted carcinogenesis presumably would continue, and some antibodies generated by a tumor may persist. Markers that do revert to normal after successful treatment could be used to follow disease recurrence and progression, as PSA (for prostate cancer) CEA (for colorectal cancer) and CA-125 (for ovarian cancer) are used now. Here again, advanced anatomical detection may aid the molecular screen to locate recurrent neoplasia that is not otherwise evident. Ideally, the validation of molecular screening markers would include study of their behavior as markers of disease progression after excision of the tumors that are detected.

In some organs, it may even be a challenge to find the cancers indicated by molecular biomarkers.

Some of the cancers detected may not need to be treated.

Do you want to know more about a molecular cancer screen many years before an actual cancer can be detected? Email motherhealth@gmail.com as need at least 25,000 people who wanted to be cancer screen early 20yrs before a real threat appears and another tests to determine the molecular age of your cells.

Prognostic biomarker is how cancer might develop for each one

Before a cancer will advance in the future, do you want to have a tests – prognostic biomarker, that will tell you how cancer will progress in the future? Would you like to know from your blood test how cancer might develop over time?

All of us do not want to be in a situation where cancer is in the last stage already and applying precision medicine to reduce cost, to reduce side effects of chemo and to target cancer with precision.

Mammaprint test (breast cancer tissues) provides a correlation with high or low outcome risk for distant metastases in patients with invasive breast cancer.

Other genetic tests using saliva and blood samples will come out soon using prognostic biomarkers to warn us of how cancer or faster cell degradation might develop in the distant future. We have to be proactive with our health before it is too late.

Email motherhealth@gmail.com if you wanted to be proactive in knowing how you can slow cancer or aging in the future and/or find prognostic biomarkers to give us time to help our body fight cancer or slow aging.

Connie

From Wiki:

A biomarker indicates a change in expression or state of a protein that correlates with the risk or progression of a disease, or with the susceptibility of the disease to a given treatment.

Before

Prognostic biomarkers indicate the likelihood of patient outcome regardless of a specific treatment.

Disease-related biomarkers give an indication of the probable effect of treatment on patient (risk indicator or predictive biomarkers), if a disease already exists (diagnostic biomarker).

Prognostic markers shows the progression of disease with or without treatment.

How such a disease may develop in an individual case regardless of the type of treatment is called prognostic biomarker.

After

Predictive biomarkers are used to help optimize ideal treatments, and indicates the likelihood of benefiting from a specific therapy.

Predictive biomarkers help to assess the most likely response to a particular treatment type.

Drug-related biomarkers indicate whether a drug will be effective in a specific patient and how the patient’s body will process it.

Biomarkers for precision oncology are typically utilized in the molecular diagnostics of chronic myeloid leukemia, colon, breast, and lung cancer, and in melanoma.

A biomarker can be a substance that is introduced into an organism as a means to examine organ function or other aspects of health. For example, rubidium chloride is used in isotopic labeling to evaluate perfusion of heart muscle. It can also be a substance whose detection indicates a particular disease state, for example, the presence of an antibody may indicate an infection.

Biomarkers can be characteristic biological properties or molecules that can be detected and measured in parts of the body like the blood or tissue. They may indicate either normal or diseased processes in the body.^[1] Biomarkers can be specific cells, molecules, or genes, gene products, enzymes, or hormones. Complex organ functions or general characteristic changes in biological structures can also serve as biomarkers.

Biomarkers also cover the use of molecular indicators of environmental exposure in epidemiologic studies such as human papilloma virus or certain markers of tobacco exposure such as 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK).

Biomarkers used for personalized medicine are typically categorized as either prognostic or predictive. An example is KRAS, an oncogene that encodes a GTPase involved in several signal transduction pathways.

In addition to long-known parameters, such as those included and objectively measured in a blood count, there are numerous novel biomarkers used in the various medical specialties. Currently, intensive work is taking place on the discovery and development of innovative and more effective biomarkers.

These “new” biomarkers have become the basis for preventive medicine, meaning medicine that recognises diseases or the risk of disease early, and takes specific countermeasures to prevent the development of disease.

Biomarkers are also seen as the key to personalised medicine, treatments individually tailored to specific patients for highly efficient intervention in disease processes. Often, such biomarkers indicate changes in metabolic processes.

The “classic” biomarker in medicine is a laboratory parameter that the doctor can use to help make decisions in making a diagnosis and selecting a course of treatment.

For example, the detection of certain autoantibodies in patient blood is a reliable biomarker for autoimmune disease, and the detection of rheumatoid factors has been an important diagnostic marker for rheumatoid arthritis (RA) for over 50 years.^[7]^[8]

For the diagnosis of this autoimmune disease the antibodies against the bodies own citrullinated proteins are of particular value. These ACPAs, (ACPA stands for Anti-citrullinated protein/peptide antibody) can be detected in the blood before the first symptoms of RA appear. They are thus highly valuable biomarkers for the early diagnosis of this autoimmune disease.^[9] In addition, they indicate if the disease threatens to be severe with serious damage to the bones and joints,^[10]^[11] which is an important tool for the doctor when providing a diagnosis and developing a treatment plan.

There are also more and more indications that ACPAs can be very useful in monitoring the success of treatment for RA.^[12]This would make possible the accurate use of modern treatments with biologicals. Physicians hope to soon be able to individually tailor rheumatoid arthritis treatments for each patient.

According to Häupl T. et al. prediction of response to treament will become the most important aim of biomarker research in medicine. With the growing number of new biological agents, there is increasing pressure to identify molecular parameters such as ACPAs that will not only guide the therapeutic decision but also help to define the most important targets for which new biological agents should be tested in clinical studies.^[13]

An NIH study group committed to the following definition in 1998: “a characteristic that is objectively measured and evaluated as an indicator of normal biologic processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention.” In the past, biomarkers were primarily physiological indicators such as blood pressure or heart rate. More recently, biomarker is becoming a synonym for molecular biomarker, such as elevated prostate specific antigen as a molecular biomarker for prostate cancer, or using enzyme assays as liver function tests. There has recently been heightened interest in the relevance of biomarkers in oncology, including the role of KRAS in CRC and other EGFR-associated cancers. In patients whose tumors express the mutated KRAS gene, the KRAS protein, which forms part of the EGFR signaling pathway, is always ‘turned on’. This overactive EGFR signaling means that signaling continues downstream – even when the upstream signaling is blocked by an EGFR inhibitor, such as cetuximab (Erbitux) – and results in continued cancer cell growth and proliferation. Testing a tumor for its KRAS status (wild-type vs. mutant) helps to identify those patients who will benefit most from treatment with cetuximab.

Biomarker

In medicine, a biomarker can be a traceable substance that is introduced into an organism as a means to examine organ function or other aspects of health. For example, rubidium chloride is used as a radioactive isotope to evaluate perfusion of heart muscle. It can also be a substance whose detection indicates a particular disease state, for example, the presence of anantibody may indicate an infection. More specifically, a biomarker indicates a change in expression or state of a protein that correlates with the risk or progression of a disease, or with the susceptibility of the disease to a given treatment.

Biochemical biomarkers are often used in clinical trials, where they are derived from bodily fluids that are easily available to the early phase researchers. A useful way of finding genetic causes of diseases such as schizophrenia has been the use of a special kind of biomarker called an endophenotype.

Other biomarkers can be based on measures of the electrical activity of the brain (using Electroencephalography (so-calledQuantitative electroencephalography (qEEG)) or Magnetoencephalography), or volumetric measures of certain brain regions (using Magnetic resonance imaging) or saliva testing of natural metabolites, such as saliva nitrite, a surrogate marker for nitric oxide. One example of a commonly used biomarker in medicine is prostate-specific antigen (PSA). This marker can be measured as a proxy of prostate size with rapid changes potentially indicating cancer. The most extreme case would be to detect mutant proteins as cancer specific biomarkers through Selected Reaction Monitoring (SRM), since mutant proteins can only come from an existing tumor, thus providing ultimately the best specificity for medical purposes.^[5]

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Tag: RNA