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Hypothesis: A motor neuron toxin produced by a clostridial species residing in gut causes ALS
Alternative Hypothesis of Neuronal Death in …
These findings provide support for the 'amyloidcascade hypothesis' as an explanation for the pathogenesis of AD,and the experimental models provide valuable tools for the testingof Aβ-modifying drugs. However, APP transgenic mice seldom presentwith NFTs and neuronal loss, which are the hallmarks of AD. Thismay be associated with the fact that multiple genes, rather thanAPP alone, are involved in the occurrence of AD and informationlearned from studies of familial AD (fAD) may not be applicable tosporadic AD (sAD) ().
The Alzheimer’s peptide Aβ is a natural cleavage product released within neuronal cells. If misfolded, Aβ forms distinct structures that are prone to aggregation, first into oligomers, then into progressively larger structures called amyloid plaques. It is now believed that Aβ oligomers are the toxic form of the peptide that may impair basic neuronal processes, such as the communication between the nerve cells, long before clinical symptoms become obvious. However, molecular details of these early processes remain largely unknown.
The mirror neuron hypothesis ..
These findings on humans were initially hailed as providing crucial empirical support for the mirror neuron theory (see for example, Christian Keysers and Valeria Gazzola, “Social Neuroscience: Mirror Neurons Recorded in Humans,” Current Biology 20.8 (April 2010): R353-R354). But the new research results have begun to complicate the picture of the function of mirror neurons, limiting their role and giving due credit to the importance of non-mirror systems. Cognitive neuroscientist Greg Hickok, a long-time critic of mirror neuron theory, sees in the theoretical revisions now being proposed by mirror neuron theorists evidence of a retreat that amounts to a confirmation of his alternative theory, according to which mirror neurons are part of the sensorimotor system involved in action selection and control, rather than action understanding.
[…] thalamus and the limbic areas, involved in the processing of emotions, are aroused, as well as the mirror neuron system. Other areas of arousal are cortical areas, involved in face and body perception, and the premotor […]
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Transgenic rats offer distinctive advantages overmice in many aspects, including rich, well-characterized behaviors,as well as being closer genetically, physiologically andmorphologically to humans than mice. Thus, great efforts have beenmade to develop models of AD in transgenic rats, as well as intransgenic mice (). Theearliest transgenic rat models of AD were developed by usingwide-type APP transgene, which exhibited an accumulation ofintracellular Aβ without extracellular senile plaques () until 17–18 months of age (,). When a human PS1 transgene wasintroduced, the resulting rats exhibited progressive plaqueaccumulation, astrocytic and microglial activation, tauhyperphosphorylation, as well as behavioral deficits related toAβ42 loads in the hippocampus, with the onset of Aβ deposition at 7months (). The firsttransgenic rat models developing progressive NFTs expressed a human3-repeat tau protein (), whichformed NFTs in neocortices at 9 months of age. Unfortunately, thismodel exhibited no neuronal damage in the hippocampus andneocortex, despite largest accumulations of tangles in theseregions.
Despite plaque and NFT formation, the APP and taudouble transgenic mice exhibited the same level of Aβ depositscompared to that in the single APP transgenic mice, indicating thatthese mouse models do not accurately reflect AD. Triple transgenicmice (3xTg-AD), expressing APP, PS1M146V and tauP301Ltransgenes, have been shown to develop extracellular Aβ depositsfrom 6 months of age and a tau-related pathology at 10-12 months ofage, which began in the hippocampus and then expanded to theneocortex, closely mimicking the development pattern of Aβ andtauopathy in the human AD brain () (). At the same time, amyloidosis and tauopathy wereaccompanied by neuronal and synaptic loss, and age-related behaviordeficits were also present prior to the development of plaques andtangle pathology (). In thismodel, microglial activation and the upregulation of inflammatorymarkers were observed at 3 months of age, in parallel with theincrease in Aβ deposits (). Itappears that this model simulates the key pathological features ofhuman AD and has the potential to be used to validate therapiestargeting the mechanisms underlying AD pathology. This model hasbeen widely used in the study of AD pathophysiology and the testingof potential therapies.
Entrainment of Arteriole Vasomotor Fluctuations ..
Coupled Oscillator Model of the Central Hypothesis
Muscle | Hypothesis | Neuron
The Amazing Neuron: Facts about Neurons - …
The neuron hypothesis
07/10/2011 · APA Reference Hale, J
assumptions and experimental methods associated with the Basic Emotions View and the mirror neuron hypothesis
The Amazing Neuron: Facts about Neurons
The intervention model was established to explorethe role of one specific neurotransmitter pathway in ADpathophysiology, and in particular to test the cholinergichypothesis of AD (). Toestablish such models, animals are subjected to intracranialinjections of chemical substances or the induction of lesions intospecific brain regions to reproduce AD (). The established modelsrepresent some characteristics of AD, such as deficits incholinergic function and learning impairments ().
Efficiency Of Brain Training | HAPPYneuron
In pathological terms, the AD-affected brain ischaracterized by widespread senile plaques of extracellular Aβpeptides, intracellular NFTs, as well as neuronal and synaptic loss(). Senile plaque iscomposed of a central core formed by Congo red-positive Aβ proteinsand degenerating nerve endings surrounding the Aβ core. NFTs areneuronal inclusions of the microtubule-associated protein (MAP) tauand consist of aggregated, hyperphosphorylated tau. In ADpathology, senile plaques and NFTs appear in the hippocampus, theentorhinal and polymodal association cortices, and the basalforebrain. These brain regions are also severely affected byneuronal and synaptic loss. In addition to the neuropathologicalchanges, there are also a number of pathophysiological disturbancesoccurring in the AD-affected brain, including inflammatoryreactions, such as angiogenesis and gliogenesis ().
Hypothesis Journal » Rewiring the stress response: A …
In order to explore more effective treatments, amore complete understanding of the pathophysiology of AD isrequired. As the pathological changes associated with AD areinitiated several years prior to the onset of clinical signs(,), it is impossible to probe the humanneuropathology at this stage. However, on the positive side, animalmodels are valuable tools which may be used to simulate thepathological changes associated with human AD and then to decipherthe pathogenesis, particularly in the pre-symptomatic stage. Inparticular, the advent of transgenic animal models, in combinationwith non-transgenic animals, has allowed researchers to conductin-depth studies of AD (,).Animal models cam reproduce the overt changes occurring in patientswith AD; however, complex conditions may limit theaccessibility to the tissue of interest and prevent real-time andspatial measurements of biological changes (). Consequently, several experimental models of AD (,),which provide detailed regional and cell-level information, havebeen developed to enhance the usefulness of animalmodels. All these models are of value for deciphering thefundamental mechanisms underlying AD pathology and also, for thetesting of novel therapies targeted against this disease.
A giant neuron has been found wrapped around the …
Progress in stem cell techniques has broadened ourhorizon for disease modeling (). For AD, disease-specificinduced pluripotent stem cell (iPSC) lines have been generated frompatients with sAD or fAD (),providing an effective approach for disease modeling and drugdiscovery. In the study by Yagi (), iPSCs were acquired from patientswith fAD with mutations in PS1 and PS2, which demonstratedincreased levels of Aβ42 in all iPSC lines, supporting the role ofAβ as an initiating factor in AD pathogenesis. Using the samemethod, Israel () generated iPSCs not only frompatients with fAD, but also sporadic cases. In their study, theiPSC-derived neurons exhibited significantly higher levels of Aβ40,phospho-tau, GSK-3β, and endosomes (). Phenotypic analysis revealed thatneurons with the genome of sAD cases exhibited the phenotypesobserved in fAD samples, suggesting that genetics plays animportant, albeit complex, role in sAD. In a previous study, whendocosahexaenoic acid (DHA) was used to treat AD iPSC-derivedneurons (), intracellular Aβloads were notably reduced in sAD and fAD AD neurons, while thestress response of neurons was alleviated in only one patient withsAD, suggesting that heterogeneity exists between patients with sADand fAD, and indicating that DHA may be effective in some patientswith AD. These results indicate that iPSCs provide a uniqueplatform for observing AD-associated phenotypes and therapeuticscreening. As iPSC lines from patients with sAD carry differentgenetic variants, the generation of sufficient stem cells isrequired to fully guide drug development and enhance ourunderstanding of AD.
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