Why do neurons die in Alzheimer’s disease?

Alzheimer’s disease, which affects around 800,000 people in Spain, causes significant loss of neurons. But the events that cause these brain cells to die remain poorly understood.

A new Northwestern Medicine study published in the journal Nature Communications suggests that RNA interference may play a key role in the development of Alzheimer’s disease.

Scientists have identified short strands of toxic RNA for the first time that contribute to brain cell death and DNA damage in aging and the Alzheimer’s brain.

In their statement, the scientists explain that short chains of protective RNA decrease with age, which can lead to the development of Alzheimer’s disease.

The study also found that older people with superior memories (known as “Super Aged People”) have more protective short strands of RNA in their brain cells. “Superagers” are people aged 80 years or older who have the memory of people 20–30 years younger.

“No one has ever linked RNA activity to Alzheimer’s disease,” said study author Marcus Peter of Northwestern University Feinberg School of Medicine.

“We discovered that In aging brain cells, the balance between toxic and protective RNAs shifts towards toxic ones.“.

The Northwestern University discovery could have implications for more than just Alzheimer’s disease. “Our data provides a new explanation why in almost all neurodegenerative diseases affected persons have decades of asymptomatic life, and then the disease gradually begins to manifest itself because cells lose their defenses as they age,” Peter said.

The results also indicate new treatment for Alzheimer’s disease

and potentially other neurodegenerative diseases.

Alzheimer’s disease is characterized by the progressive appearance of beta-amyloid plaques, deposits that form toxic plaques between neurons, neurofibrillary tangles (tau), scarring, and ultimately the death of brain cells.

“The enormous investment in Alzheimer’s drug development has focused on two mechanisms: reducing the amyloid plaque burden in the brain (which is the hallmark of Alzheimer’s disease diagnosis and accounts for 70 to 80% of the effort) and preventing phosphorylation or tau tangles,” Peter said . .

“However, treatments aimed at reducing the number of amyloid plaques have not yet resulted in an effective and well-tolerated treatment.

“Our data supports the idea that stabilize or increase the number of short protective RNAs in the brain there may be a completely new approach to stop or delay Alzheimer’s disease or neurodegeneration in general.

If confirmed, improvements could occur in the near future, as stated medicines existsaid Peter, but they will need to be tested in animal models and refined.

The next step in Peter’s research is to determine in various animal and cellular models (as well as in the brains of Alzheimer’s patients) the exact contribution of toxic RNAs to the cell death observed in the disease, and to find better compounds that selectively increase levels of protective RNAs or block the effects of toxins.