Development and psychometric evaluation of a brief version of the hyperventilation questionnaire: the HVQ-B.

The fear of arousal sensations characterizes some anxiety disorders and is a core feature of an established risk factor for anxiety and related disorders (i.e. anxiety sensitivity; Taylor, 1999). Anxiety sensitivity (AS) refers to a fear of anxiety-related bodily sensations stemming from beliefs that these have catastrophic consequences. Interoceptive exposure (IE; repeated exposure to feared arousal sensations) has been shown to decrease AS. The 33-item Hyperventilation Questionnaire (HVQ; Rapee & Medoro, 1994) measures state levels of cognitive, affective, and somatic responses to IE and arousal induction exercises more generally. The aim of the present set of studies was to develop and evaluate a brief version of the HVQ, the HVQ-B, in order to facilitate its use in research and clinical settings. In Study 1, three existing data sets that used the long version of the HVQ were combined to select the items to be retained for the HVQ-B. In Study 2, the 18-item HVQ-B was administered and its psychometric properties were evaluated. In Study 3, a confirmatory factor analysis (CFA) was performed on the 18 items of the HVQ-B. The HVQ-B demonstrated excellent psychometric properties, and accounted for most of the variance of the questionnaire's longer version. CFA indicated a reasonably good fit of the three-factor measurement model. Finally, the HVQ-B was able to distinguish between responses to arousal induction exercises by high versus low AS participants. The HVQ-B is a useful tool to assess cognitive, affective, and somatic responsivity to arousal sensations in both research and practice.

Alzheimer's neuroborreliosis with trans-synaptic spread of infection and neurofibrillary tangles derived from intraneuronal spirochetes.

In the realm of dementia, it is astonishing to note that neurofibrillary tangles (NFT) are microscopically identical in a childhood illness (SSPE) and in a dementia of late adult life (Alzheimer's disease). The words "Alzheimer-type" NFT in peer reviewed scientific articles written by acknowledged experts underscore the striking similarities in "tangles" in two different diseases. Subacute Sclerosing Panencephalitis (SSPE) is caused by infection with atypical measles virus. Alzheimer's disease has no known cause. There is little controversy in suggesting that all of the Tangles in SSPE infected neurons are produced by slow viral type variant of Measles infection. But the mere suggestion that infection might be a cause of Alzheimer's disease confounds the establishment. If a good case is to be made for infection in Alzheimer's disease, an excellent nerve cell infection model is needed. Monkeys have provided a very reasonable model. Recently, a primate neuroborreliosis brain infection model demonstrated that Borrelia injected into the skin of monkeys resulted in the appearance of Borrelia transcriptomes in brain neurons. If Borrelia can travel from skin to brain in the monkey, then why not look at human Alzheimer's tissues to see if the DNA of Borrelia is present in the human brain? The molecular detection tools perfected in animal neuroborreliosis studies have been applied to human Alzheimer's disease brain tissues. Seven of ten cases of Alzheimer's disease from McLean Hospital Brain Bank of Harvard University yielded positive signals for infectious DNA in a small pilot study. Alzheimer's diseased neurons analyzed with DNA probes, produced little "dots" of positive staining. Granulovacuolar bodies in Alzheimer's diseased neurons (little dots in a bubble), are one of the expected microscopic profiles of Alzheimer's disease. "Little dots" inside nerve cells are also signatures of viral infectious agents inside of nerve cells. So with the assistance of the microscope and the tools of molecular biology, a new model of infection emerges as a cause of "Alzheimer's-type" neurofibrillary tangles. Here I hypothesize that it is chronic infection of human neurons in Alzheimer's disease that produces neurofibrillary tangles by a pathway similar to the chronic SSPE infection tangle pathway. In addition, transmission of infection from nerve to nerve is proposed to explain the evolution of Alzheimer's disease. Herein is offered a new view for the origins and for the progression of diseased nerves with tangle formations in Alzheimer's disease based on infection.

Alzheimer's disease Braak Stage progressions: reexamined and redefined as Borrelia infection transmission through neural circuits.

Brain structure in health is a dynamic energized equation incorporating chemistry, neuronal structure, and circuitry components. The chemistry "piece" is represented by multiple neurotransmitters such as Acetylcholine, Serotonin, and Dopamine. The neuronal structure "piece" incorporates synapses and their connections. And finally circuits of neurons establish "architectural blueprints" of anatomic wiring diagrams of the higher order of brain neuron organizations. In Alzheimer's disease, there are progressive losses in all of these components. Brain structure crumbles. The deterioration in Alzheimer's is ordered, reproducible, and stepwise. Drs. Braak and Braak have described stages in the Alzheimer disease continuum. "Progressions" through Braak Stages benchmark "Regressions" in Cognitive function. Under the microscope, the Stages of Braak commence in brain regions near to the hippocampus, and over time, like a tsunami wave of destruction, overturn healthy brain regions, with neurofibrillary tangle damaged neurons "marching" through the temporal lobe, neocortex and occipital cortex. In effect the destruction ascends from the limbic regions to progressively destroy the higher brain centers. Rabies infection also "begins low and finishes high" in its wave of destruction of brain tissue. Herpes Zoster infections offer the paradigm of clinical latency of infection inside of nerves before the "marching commences". Varicella Zoster virus enters neurons in the pediatric years. Dormant virus remains inside the neurons for 50-80 years, tissue damage late in life (shingles) demonstrates the "march of the infection" down neural pathways (dermatomes) as linear areas of painful blisters loaded with virus from a childhood infection. Amalgamation of Zoster with Rabies models produces a hybrid model to explain all of the Braak Stages of Alzheimer's disease under a new paradigm, namely "Alzheimer's neuroborreliosis" in which latent Borrelia infections ascend neural circuits through the hippocampus to the higher brain centers, creating a trail of neurofibrillary tangle injured neurons in neural circuits of cholinergic neurons by transsynaptic transmission of infection from nerve to nerve.

Spirochetal cyst forms in neurodegenerative disorders,...hiding in plain sight.

Here is proposed a hypothesis that a completely unsuspected biology exists for pathogenic spirochetes, namely that the cystic spirochetal forms (long thought to be static and resting or just a dormant cohort) actually are capable of killing mammalian host cells. At least two "lethal" scenarios are proposed; first, the host cell destruction from the "inside out" by small caliber cystic forms invading the host cell cytoplasm, and second host cell destruction by engulfment of entire host cells by large caliber cystic spirochetal forms. Conventional thinking about spirochetal cyst forms is divided between two polar spheres of influence; one a majority community that completely denies the existence of spirochetal cyst forms, and a second group of academically persecuted individuals who accepts the precepts of such antebellum scientists as Schaudinn, Hoffman, Dutton, Levaditi, Balfour, Fantham, Noguchi, McDonough, Hindle, Steiner, Ingraham, Coutts, Hampp, Warthin, Ovcinnikov, and Delamater. Microscopic images of cystic spirochetes are difficult to ignore, but as has been the case in this century, academic "endowments" have nearly expunged all cystic spirochetal image data from the current textbook versions of what is the truth about the spirochetaceae. If the image database from the last century is obliterated; many opportunities to diagnose will be lost. Variously sized cystic spirochetal profiles within diseased nerve cells explain the following structures: Lewy body of Parkinson's disease, Pick body, ALS spherical body, Alzheimer plaque. Borrelia infection is therefore a unifying concept to explain diverse neurodegenerative diseases, based not entirely on a corkscrew shaped profile in diseased tissue, but based on small, medium and large caliber rounded cystic profiles derived from pathogenic spirochetes which are..."hiding in plain sight".

A life cycle for Borrelia spirochetes?

Subsequent to Schaudinn and Hoffman's visualization of Treponema pallidum in 1905, many distinguished syphilologists proposed that spirochetes have a life cycle. What is the "essence" of a life cycle? Simply put, life cycles are diverse arrays of life forms, which emerge in an ordered sequence; which are "connected" to one another across primary and secondary hosts, and constitute a cycle with "circular" relationship between hosts. Fecal-oral life cycles and blood-to-blood life cycles are exemplary of host parasite relationships in this realm. The "blood-to-blood" begins and ends with an insect taking a blood "meal". In this operatic scenario, a "blood-less" insect functions simultaneously as a hypodermic needle and as an incubator for some of the infectious components. The initial phase is inside the body fluid compartment of an insect. The second phase is in the blood or body fluid of a warm-blooded mammal. Third, is the phase inside the cell of a mammalian host. And a final portion of the "life" marked by "death" of the parasitized mammalian cells and the release of infectious parasites which return to the "warm" blood where the "cold blooded" vector again takes a blood meal. The cycle then begins again. In each phase of a blood to blood life cycle, the infectious agent changes its shape. Blood phase "profiles" look different from "tissue phase" profiles. Some of the tissue phase profiles may be "invisible". Borrelia spirochetes offer an excellent example of a life cycle, by virtue of the insect vector to mammalian "piece", the blood and intracellular residence "pieces" and the morphologic diversity "piece". Stereotypes of what a spirochete "should " look like, have actually produced a state of "perseveration" in spirochetal pathobiology. We have been "stuck" like a broken record, on the corkscrew form, and have failed to see the rest of the life cycle. Cystic, granular, and cell wall deficient spirochetal profiles, which were well known in the 19th and 20th centuries by such titans as Schaudinn, Hoffman, Noguchi, Delamater, Steiner, and Mattman, have been repudiated by professional microbiologists, and by pathologists who practice and who confer the status of 21st century truths in microbiology matters. Proper microscopic study, as is required by Dr. Robert Koch's second postulate, for establishing links between microbes and disease, presupposes that the microscopist be aware of the complete array of morphologic repertoires of the alleged pathogen. (Morphologies, which are herein introduced.).

Plaques of Alzheimer's disease originate from cysts of Borrelia burgdorferi, the Lyme disease spirochete.

Here is hypothesized a truly revolutionary notion that rounded cystic forms of Borrelia burgdorferi are the root cause of the rounded structures called plaques in the Alzheimer brain. Rounded "plaques' in high density in brain tissue are emblematic of Alzheimer's disease (AD). Plaques may be conceptualized as rounded "pock mark-like" areas of brain tissue injury. In this century, in brain tissue of AD, plaques are Amyloid Plaques according to the most up to date textbooks. In the last century, however, Dr. Alois Alzheimer did not require amyloid as the pathogenesis for either the disease or for the origin of its plaques. Surely, amyloid is an event in AD, but it may not be the primal cause of AD. Indeed in plaques, amyloid is regularly represented by the "congophilic core" structure which is so named because the waxy amyloid material binds the congo red stain and is congophilic. However an accepted subset of plaques in AD is devoid of a congophilic amyloid core region (these plaques "cotton wool" type plaques, lack a central congophilic core structure). Furthermore, there is "plaque diversity" in Alzheimer's; small, medium and large plaques parallel variable cystic diameters for Borrelia burgdorferi. Perturbations of AD plaque structure (i.e. young plaques devoid of a central core and older plaques with or without a central core structure) offer room for an alternate pathway for explanation of ontogeny of the plaque structures. If amyloid is not required to initiate all of the possible plaques in Alzheimer's, is it possible that amyloid just a by product of a more fundamental primal path to dementia? If a byproduct status is assigned to amyloid in the realm of plaque formation, then is amyloid also an epiphenomenon rather than a primary pathogenesis for Alzheimer's disease. In the "anatomy is destiny" model, cysts of borrelia are always round. Why then not accept roundness as a fundamental "structure determines function" argument for the answer to the mystery of why Alzheimer plaques are always round? Parataxis causality, a concept borrowed from philosophy, is the error that comes from linking two events, which occur contemporaneously or in close proximity to one another with a cause and effect relationship. Parataxis tells us that what appears to be cause and effect in the couplet "amyloid plaque" merely by a proximity relationship may be "spurious causality" which is a cognitive dead end.

Transfection "Junk" DNA - a link to the pathogenesis of Alzheimer's disease?

A transfection product incorporates in one molecule of human DNA, an inserted segment of DNA from another species. This communication addresses the hypothesis that a novel variation of the theme of transfection, namely "junk transfection" for which no protein product and no RNA is transcribed, might offer insights into the pathogenesis of Alzheimer's disease. It is hypothesized that spirochetal DNA gains access to the intracellular compartment of nerve cells during the subclinical latency phase of neuroborreliosis and chemically combines with human DNA. A previously reported Molecular interrogation of Alzheimer's disease autopsy tissues has yielded novel DNA sequences containing the 11 q human chromosome and a short piece of the Borrelia burgdorferi Flagellin B DNA. Although the usually encountered transfection product bundles an entire nonhuman gene within it, this model proposes that shorter inserts into the human genome constitute "junk transfection" because no protein is derived from them. Junk transfections would offer an important new cognitive model for the detection of occult infections as the root causes for the Tauopathies, which are degenerative neurological disorders, including Alzheimer's disease.