Состоятельность диагностики нейродегенеративных заболеваний


Я привожу обыкновенную википедическую статью
Signs and symptoms[edit]
Symptoms of CTE generally begin 8–10 years after experiencing repetitive mild traumatic brain injury.[2] First stage symptoms include deterioration in attention as well as disorientation, dizziness, and headaches. Further disabilities appear with progressive deterioration, including memory loss, social instability, erratic behavior, and poor judgment. Third and fourth stages include progressive dementia, slowing of muscular movements, hypomimia, impeded speech, tremors, vertigo, deafness, and suicidality. Additional symptoms include dysarthria, dysphagia, and ocular abnormalities - such as ptosis.[3]

Currently, CTE can only be definitively diagnosed by direct tissue examination, including full autopsies and immunohistochemical brain analyses.[4]

The neuropathological appearance of CTE is distinguished from other tauopathies, such as Alzheimer's disease. The four clinical stages of observable CTE disability have been correlated with tau pathology in brain tissue, ranging in severity from focal perivascular epicentres of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions.[5]

The primary physical manifestations of CTE include a reduction in brain weight, associated with atrophy of the frontal and temporal cortices and medial temporal lobe. The lateral ventricles and the third ventricle are often enlarged, with rare instances of dilation of the fourth ventricle.[6] Other physical manifestations of CTE include anterior cavum septi pellucidi and posterior fenestrations, pallor of the substantia nigra and locus ceruleus, and atrophy of the olfactory bulbs, thalamus, mammillary bodies, brainstem and cerebellum.[7] As CTE progresses, there may be marked atrophy of the hippocampus, entorhinal cortex, and amygdala.[2]

On a microscopic scale the pathology includes neuronal loss, tau deposition, TAR DNA-binding Protein 43 (TDP 43)[5] beta-amyloid deposition, white matter changes, and other abnormalities. The tau deposition occurs as dense neurofibrillary tangles (NFT), neurites, and glial tangles, which are made up of astrocytes and other glial cells[6] Beta-amyloid deposition is a relatively uncommon feature of CTE.

A small group of individuals with CTE have chronic traumatic encephalomyopathy (CTEM), characterized by motor neuron disease symptoms and mimics Amyotrophic Lateral Sclerosis (ALS). Progressive muscle weakness and balance and gait problems seem to be early signs of CTEM.[6]

Exosome vesicles created by the brain are potential biomarkers of TBI, including chronic traumatic encephalopathy.[8]

The lack of in-vivo techniques to show distinct biomarkers for CTE is the reason CTE cannot currently be diagnosed during lifetime. The only known diagnosis for CTE occurs by studying the brain tissue after death. Concussions are non-structural injuries and do not result in brain bleeding, which is why most concussions cannot be seen on routine neuroimaging tests such as CT or MRI.[9] Acute concussion symptoms (those that occur shortly after an injury) should not be confused with CTE. Differentiating between prolonged post-concussion syndrome (PCS, where symptoms begin shortly after a concussion and last for weeks, months, and sometimes even years) and CTE symptoms can be difficult. Research studies are currently examining whether neuroimaging can detect subtle changes in axonal integrity and structural lesions that can occur in CTE.[2] Recently, more progress in in-vivo diagnostic techniques for CTE has been made, using DTI, fMRI, MRI, and MRS imaging; however, more research needs to be done before any such techniques can be validated.[6]

PET tracers that bind specifically to tau protein are desired to aid diagnosis of CTE in living individuals. One candidate is the tracer [18F]FDDNP, which is retained in the brain in individuals with a number of dementing disorders such as Alzheimer's disease, Down syndrome, progressive supranuclear palsy, familial frontotemporal dementia, andCreutzfeld–Jakob disease.[10] In a small study of 5 retired NFL players with cognitive and mood symptoms, the PET scans revealed accumulation of the tracer in their brains.[11]However, [18F]FDDNP, binds not only to tau but to beta-amyloid and other proteins as well. Moreover, the sites in the brain where the tracer was retained were not consistent with the known neuropathology of CTE.[12] A more promising candidate is the tracer [18F]-T807, which binds only to tau. It is being tested in several clinical trials.[12]

A putative biomarker for CTE is the presence in serum of autoantibodies against the brain. The autoantibodies were detected in football players who experienced a large number of head hits but no concussions, suggesting that even sub-concussive episodes may be damaging to the brain. The autoantibodies may enter the brain by means of a disrupted blood-brain barrier, and attack neuronal cells which are normally protected from an immune onslaught.[13] Given the large numbers of neurons present in the brain, and considering the poor penetration of antibodies across a normal blood-brain barrier, there is an extended period of time between the initial events (head hits) and the development of any signs or symptoms. Nevertheless, autoimmune changes in blood of players may consist the earliest measurable event predicting CTE.[14]

Robert A. Stern, one of the scientists at the Boston University CTE Center,[15] said in 2015 that "he expected a test to be developed within a decade that will be able to diagnose C.T.E. in living people".[16]

Как посчитать темных кошек в темной комнате их там нет, или нету метода подсчета

МРТ 3ТСЛ +контраст несостоятельна и не исключает целый пласт патологий

от вегетососудистой дистании до шизофрении.... мы не можем посчитать котов, все это темная комната
где область психиатрии - иммунологии, клеточной патологии, обмена веществ или объемной - патологии последняя визуализируется
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Ветеран форума
Ну так и есть, все верно. Диагнозы в этой сфере ставятся чаще всего не этиологические, а "симптоматические", типа "что вижу, то пою". Проявляется так - назовём таким именем, проявляется иначе - другим. "Лечение" тоже главным образом направлено на симптомы. В причины никто особо и не стремится вникать.
Разве что случаи, когда что-то точно визуализируется.
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