New Mechanism by Which Alzheimer’s Spreads Through the Brain

Summary: According to researchers, exosomes can transport toxic aggregates of amyloid beta to new neurons in the brain.

Source: Linkoping University.

The waste-management system of the cell appears to play an important role in the spread of Alzheimer’s disease in the brain. A new study has focused on small membrane-covered droplets known as “exosomes”. It was long believed that the main task of exosomes was to help the cell to get rid of waste products. In simple terms, they were thought of as the cell’s rubbish bags. However, our understanding of exosomes has increased, and we now know that cells throughout the body use exosomes to transmit information. It’s now known that the exosomes can contain both proteins and genetic material, which other cells can absorb.

The Linköping researchers have shown in the new study that exosomes can also transport toxic aggregates of the protein amyloid beta, and in this way spread the disease to new neurons. Aggregated amyloid beta is one of the main findings in the brains of patients with Alzheimer’s disease, the other being aggregates of the protein tau. As time passes, they form ever-increasing deposits in the brain, which coincides with the death of nerve cells. The cognitive functions of a person with Alzheimer’s disease gradually deteriorate as new parts of the brain are affected.

“The spread of the disease follows the way in which parts of the brain are anatomically connected. It seems reasonable to assume that the disease is spread through the connections in the brain, and there has long been speculation about how this spread takes place at the cellular level,” says Martin Hallbeck, associate professor in the Department of Clinical and Experimental Medicine at Linköping University and senior consultant of clinical pathology at Linköping University Hospital.

In a collaboration with researchers at Uppsala University, he and his co-workers have investigated exosomes in brain tissue from deceased persons. The research team at Linköping University found more amyloid beta in exosomes from brains affected by Alzheimer’s disease than in healthy controls. Furthermore, the researchers purified exosomes from the brains from people with Alzheimer’s disease, and investigated whether they could be absorbed by cells cultured in the laboratory.

the researcher looking through a microscope
Researchers at Linköping University study how Alzheimer’s disease spreads in the brain. image is credited to Thor Balkhed/Linköping University.

“Interestingly, exosomes from patients were absorbed by cultured neurons, and subsequently passed on to new cells. The cells that absorbed exosomes that contained amyloid beta became diseased,” says Martin Hallbeck.

The researchers treated the cultured neurons with various substances that prevent exosomes from being formed, released, or absorbed by other cells. They were able to reduce the spread of the aggregated amyloid beta between cells by disrupting the mechanism in these ways. The methods used in these laboratory experiments are not yet suitable for treating patients, but the discovery is important in principle. “Our study demonstrates that it is possible to influence this pathway, and possibly develop drugs that could prevent the spreading. The findings also open up the possibility of diagnosing Alzheimer’s disease in new ways, by measuring the exosomes,” says Martin Hallbeck.

About this neuroscience research article

Funding: The research has received financial support from donors that include the Swedish Research Council, the Swedish Alzheimer’s Foundation, and the Swedish Brain Foundation.

Source: Karin Söderlund Leifler – Linkoping University
Publisher: Organized by
Image Source: image is credited to Thor Balkhed/Linköping University.
Original Research: Open access research for “Alzheimer’s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers” by Maitrayee Sardar Sinha, Anna Ansell-Schultz, Livia Civitelli, Camilla Hildesjö, Max Larsson, Lars Lannfelt, Martin Ingelsson, and Martin Hallbeck in Acta Neuropathologica. Published June 13 2018

Cite This Article

[cbtabs][cbtab title=”MLA”]Linkoping University “New Mechanism by Which Alzheimer’s Spreads Through the Brain.” NeuroscienceNews. NeuroscienceNews, 13 June 2018.
<>.[/cbtab][cbtab title=”APA”]Linkoping University (2018, June 13). New Mechanism by Which Alzheimer’s Spreads Through the Brain. NeuroscienceNews. Retrieved June 13, 2018 from[/cbtab][cbtab title=”Chicago”]Linkoping University “New Mechanism by Which Alzheimer’s Spreads Through the Brain.” (accessed June 13, 2018).[/cbtab][/cbtabs]


Alzheimer’s disease pathology propagation by exosomes containing toxic amyloid-beta oligomers

The gradual deterioration of cognitive functions in Alzheimer’s disease is paralleled by a hierarchical progression of amyloid-beta and tau brain pathology. Recent findings indicate that toxic oligomers of amyloid-beta may cause propagation of pathology in a prion-like manner, although the underlying mechanisms are incompletely understood. Here we show that small extracellular vesicles, exosomes, from Alzheimer patients’ brains contain increased levels of amyloid-beta oligomers and can act as vehicles for the neuron-to-neuron transfer of such toxic species in recipient neurons in culture. Moreover, blocking the formation, secretion or uptake of exosomes was found to reduce both the spread of oligomers and the related toxicity. Taken together, our results imply that exosomes are centrally involved in Alzheimer’s disease and that they could serve as targets for development of new diagnostic and therapeutic principles.

Feel free to share this Neuroscience News.
Join our Newsletter
I agree to have my personal information transferred to AWeber for Neuroscience Newsletter ( more information )
Sign up to receive our recent neuroscience headlines and summaries sent to your email once a day, totally free.
We hate spam and only use your email to contact you about newsletters. You can cancel your subscription any time.
  1. I’m very far noone was able to diagnose me.I was a growing up in communizm.raised in daycares,camps missing my mother tremendously.I never fit in vry scared of my the point ,started loosing myself what to do ,he be home soon,than I heard the special thoose camp I developed the most awful feeling,wich was triggered due to my husband lett for a young girl leaving me w.3 children.while being structured raising them was all good,very busy .They left graduated. Now I’m 68 with a child trappt inside.can’t handle any assuming falsely of me.unkindness,coming from loved ones noone understands (if they not kind, rough t o my needs ignore helping in my age limitations,snap at me etc THAT CHILDHOOD FEELING PUPPY UP ,I BREAK DOWN LOOSING ALL ENERGY FALLING ASLEEP WHILE EATING TEXTING ,ANYTHIME,ANYWHERE.IT TAKES HARDER AND HARDER TO START FUNCTIONING AGAIN.I’M A COMMON SRNCE,A THINKER, PGOBLEMSOLVER,INVENTOR SUPER SENSETIVE TO NEEDS,BEAUTY, God, music – my med- dancing,I care much,vllunteer,.but no more since I just can’t control myself when this thing hits me become that child long ago I was SOOO LOST,ALONE I’M NO GOOD TO NOONE .WANT TO BE BEST GR.MA.BREAKS ME THAT I CAN’T BE.ANTIDEPRESSANT S NO HELP.COUNCILLOR NOT EIGHTER. SELFCONTROLL,PRAY LITTLE HELP WHEN STATS BUT CAN’T HOLD ON. BECOME TOTALLY LOST.TOLD FAMILY ALL WD NEED IS PREVENT .PLEASE TREAT ME KIND WATCH IT A LITTLE.DON’T BELIEVE MY WORDS AT ALL

Comments are closed.