Summary: Researchers have devised a new, non-invasive method for tracking the progression of Alzheimer’s disease. The study also proposes removing excess toxic Alzheimer’s proteins from the blood could improve clinical symptoms and pathologies of Alzheimer’s disease.
Source: University of Malaga
A new study conducted by University of Malaga researcher Inés Moreno, in collaboration with the University of Texas, has identified a potential non-invasive therapy that could check the progress of Alzheimer’s disease, the major form of dementia in the elderly population.
In a preclinical model, Moreno has managed to reduce the amount of toxic proteins in the brain—the aggregate of which is the main cause of neuronal death in Alzheimer’s disease.
These proteins are also present in blood, and according to Moreno, they are in equilibrium with the brain—if they increase in the brain, they increase in the blood, and vice versa. Based on these results, Moreno proposes removing these toxic aggregates as a target for Alzheimer’s disease therapy.
The paper was published by the scientific journal Molecular Psychiatry.
“Removing the toxic proteins from the brain is the goal of most of the current therapies for Alzheimer’s disease,” explains Moreno, who is part of the UMA group NeuroAD.
Acting at a circulatory level
The innovation of this research is that it proposes reducing these toxins from the blood, as they are also present in the bloodstream.
“We have verified that if we remove toxins from the blood, they drain again from brain to blood in search of equilibrium, improving the clinical signs and pathology of the disease,” says Moreno.
The scientist points out that nowadays the analysis of blood samples is already used, in some cases, for the diagnosis of the disease as an alternative to neuroimaging.
However, so far it has never been used for the purpose proven in this paper. Consequently, this new use “opens the door to potential non-invasive therapeutic strategies to be implemented at a circulatory level.”
The results, as evidenced in animal models, show that this treatment could improve memory and learning capacity as well as correct cognitive impairments, being able not only to remove toxic proteins, but also modify key factors in the development of this disease.
The University of Texas, where Inés Moreno is also an associate professor, will continue with this study at a clinical level, seeking to determine the molecular mechanisms involved in improvement of the disease. The research also seeks to address whether the treatment would work in patients by means of, for instance, dialysis or even transfusions in patients with dementia.
Preventive and therapeutic reduction of amyloid deposition and behavioral impairments in a model of Alzheimer’s disease by whole blood exchange
Alzheimer’s disease (AD) is the major form of dementia in the elderly population. The main neuropathological changes in AD patients are neuronal death, synaptic alterations, brain inflammation, and the presence of cerebral protein aggregates in the form of amyloid plaques and neurofibrillary tangles.
Compelling evidence suggests that the misfolding, aggregation, and cerebral deposition of amyloid-beta (Aβ) plays a central role in the disease. Thus, prevention and removal of misfolded protein aggregates is considered a promising strategy to treat AD.
In the present study, we describe that the development of cerebral amyloid plaques in a transgenic mice model of AD (Tg2576) was significantly reduced by 40–80% through exchanging whole blood with normal blood from wild type mice having the same genetic background. Importantly, such reduction resulted in improvement in spatial memory performance in aged Tg2576 mice.
The exact mechanism by which blood exchange reduces amyloid pathology and improves memory is presently unknown, but measurements of Aβ in plasma soon after blood exchange suggest that mobilization of Aβ from the brain to blood may be implicated.
Our results suggest that a target for AD therapy may exist in the peripheral circulation, which could open a novel disease-modifying intervention for AD.