The neuropathological appearance of<unk>  is distinguished from other tauopathies, such as Alzheimer's disease. The four clinical stages of observable<unk>  disability have been correlated with tau pathology in brain tissue, ranging in severity from focal perivascular epicenters of neurofibrillary tangles in the frontal neocortex to severe tauopathy affecting widespread brain regions. The primary physical manifestations of<unk>  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. Other physical manifestations of<unk>  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. As<unk>  progresses, there may be marked atrophy of the hippocampus, entorhinal cortex, and amygdala. On a microscopic scale, a pathognomonic<unk>  lesion involves p-tau aggregates in neurons, with or without thorn-shaped astrocytes, at the depths of the cortical sulcus around a small blood vessel, deep in the parenchyma, and not restricted to the subpial and superficial region of the sulcus; the pathognomonic lesion must include p-tau in neurons to distinguish<unk>  from ARTAG. Supporting features of<unk>  are: superficial neurofibrillary tangles (NFTs); p–tau in CA2 and CA4 hippocampus; p-tau in: mammillary bodies, hypothalamic nuclei, amygdala, nucleus accumbens, thalamus, midbrain tegmentum, nucleus basalis of Meynert, raphe nuclei, substantia nigra and locus coeruleus; p-tau thorn-shaped astrocytes (TSA) in the subpial region; p-tau dot-like neurites. Purely astrocytic perivascular p-tau pathology represents ARTAG and does not meet the criteria for<unk> . Beta-amyloid is not a feature of<unk> , however a person with<unk>  may have comorbid pathologies such as Alzheimer's disease. A small group of individuals with<unk>  have<unk><unk>  encephalomyopathy <unk> M), which is characterized by symptoms of motor-neuron disease and which mimics amyotrophic lateral sclerosis (ALS). Progressive muscle weakness and balance and gait problems (problems with walking) seem to be early signs of<unk> M. Exosome vesicles created by the brain are potential biomarkers of TBI, including<unk> . Loss of neurons, scarring of brain tissue, collection of proteinaceous senile plaques, hydrocephalus, attenuation of the corpus callosum, diffuse axonal injury, neurofibrillary tangles, and damage to the cerebellum are implicated in the syndrome. Neurofibrillary tangles have been found in the brains of dementia pugilistica patients, but not in the same distribution as is usually found in people with Alzheimer's. One group examined slices of brain from patients having had multiple mild<unk>  brain injuries and found changes in the cells' cytoskeletons, which they suggested might be due to damage to cerebral blood vessels. Increased exposure to concussions and subconcussive blows is regarded as the most important risk factor. This exposure can depend on the total number of fights, number of knockout losses, the duration of career, fight frequency, age of retirement, and boxing style.
Chronic traumatic encephalopathy
Parkinson's disease
Wernicke encephalopathy
Alzheimer's disease
Powassan encephalitis
Posterior reversible encephalopathy syndrome
Toxic encephalopathy
Viral encephalitis