A new study from the University of Kentucky described a novel form of dementia, is characterized by the toxic accumulation of four different proteins in the brain. Studies show many patients with a diagnosis of Alzheimer’s disease can suffer from this another and more complex neurodegenerative condition.
Alzheimer’s disease usually determined by the harmful substances of the two kinds of proteins in the brain of beta-amyloid in plaques and Tau in neurofibrillary tangles. Almost every treatment developed in recent years, to try to stop or reverse the accumulation of these toxic proteins not humansmany researchers have looked at Novel hypotheses for try your best to understand the origins of Alzheimer’s disease.
Last year in historical research is described new form of dementia based on the abnormal aggregation of a protein called TDP-43. The disease was named limbic-predominant age of TDP-43 encephalopathy, or later, and the researchers suggested that some 20 per cent of cases of Alzheimer’s disease may be misdiagnosed latter cases.
“One of the things that we learned in the last ten years or so that a lot of people that we think of dementia from Alzheimer’s, is actually there,” explains Eric Abner, one of the leading researchers of the new University of Kentucky study. “There are other brain diseases that cause the same symptoms as Alzheimer’s disease, including what we just recently found out was not.”
The new study examined data on autopsy of the brain of the 375 patients, who are in a long-term project called the University of Kentucky Alzheimer’s Disease center brain Bank. All items to donate brain tissue were followed closely for more than ten years before his death.
The researchers looked at the accumulation not only of beta-amyloid, Tau and TDP-43, but also alpha-synuclein protein, as you know, going into toxic structures called Lewy bodies. These Lewy Body the main pathological cause of neurodegeneration in Parkinson’s disease.
The results showed that about 20 percent of all subjects with dementia at the time of death signs of accumulation of all four types of toxic proteins. And those who have all four of these conditions are most severe symptoms of dementia.
“They were all causing neurodegeneration pathology that we know of. There wasn’t a word for it, so we invented one: quadruple misfolded proteins, or BIC,” says Ebner.
Individuals with BIC seen to progress from mild cognitive impairment (MCI) to dementia faster than subjects with three or fewer abnormalities. It is unclear exactly how these four pathological features interact with each other, but the researchers note that autopsy data indicate beta-amyloid accumulation may be preceded by anomalous concentrations of three other proteins. Does this mean that the amyloid plaques actively stimulate the subsequent accumulation of other proteins is not known at this stage.
Abner said that the results of his team will complicate the study of Alzheimer’s disease, offering treatment, focused on one of these pathologies may not take into account other degenerative processes, which seem to be of dementia associated with the disease. First later, but for now, BICK, these new categories of dementia are increasingly making it clear to later-life cognitive impairment and comorbidities are more diverse than previously thought.
“This is not good news, since it means that even if we could cure Alzheimer’s, we’re still dealing with TDP-43 and alpha-synuclein, and they are often found in the elderly,” says Ebner. “But we need to understand exactly what we are facing when we are trying to stop the dementia. We still have so much to learn”.
The new study was published in the journal JAMA neurology.
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