Health Spain , Burgos, Wednesday, May 22 of 2013, 13:30

The origin of Alzheimer’s disease may be in Homo sapiens’ evolution

A study published in Journal of Alzheimer’s Disease suggests that our vulnerability to neurodegenerative conditions is a price to be paid for our cognitive abilities

Cristina G. Pedraz/DICYT Emiliano Bruner, researcher at the Centro Nacional de Investigación sobre la Evolución Humana (CENIEH) –a research center on human evolution in Burgos, Spain-, and Heidi Jacobs, from the Forschungszentrum Jülich –an institute of neuroscience and medicine in Germany-, have published an article in Journal of Alzheimer’s Disease suggesting that vulnerability to neurodegenerative processes in our species, Homo sapiens, would be “the price to be paid for our cognitive abilities”. The hypothesis developed by both scientists incorporates information from paleoneurology (the study of the brain and the intracranial system by analysis of fossils), image analysis, comparative anatomy and neurophysiology.

According to Bruner, this stance was the encounter of a paleoneurologist specialized in brain anatomy and human evolution and a neuropsychologist specialized in Alzheimer’s disease (AD) and metabolism, an attempt to propose “an evolutionary framework to neurodegenerative conditions associated to a disease considered to be very destructive and increasingly present in our society”.

The researcher says that although AD is known by damages to the structure of the brain cortex areas associated with frontal and temporal lobes, it was recently revealed that the process begins with metabolic problems in deep parietal areas. “These are the same areas that, according to fossil and paleoneurological records, have visible changes related to the origin of our species, Homo sapiens; and, taking into account that this condition is only known in our species, we need to consider a relationship between both elements”, he explains. Therefore, it is necessary to assess whether anatomical changes characterizing Homo sapiens’ origin, despite cognitive advantages, may have also led to “side effects”.

“Increased neural mass; differences in geometric and spatial organization; increased energy, repair, metabolic activation and vascular activation expenditures may have set a situation of vulnerability and excess load producing weakness in deep parietal areas and functional damages”, the scientist stated; he also explained that this would be the source of vulnerability to neurodegenerative processes and, consequently, to the idea that “that is the price to be paid for our cognitive faculties”.

How come evolution did not “give up” these vulnerabilities? The answer is easy to the researcher. “Since AD is linked to non-reproductive life stages, as a side effect it does not directly affect natural selection criteria, it has silently slip through evolution’s filter”.

A New Approach

Regarding the relevance of the study, Bruner warns that the evolutionary perspective does not provide direct solutions to develop biomedical treatments, but it offers a different approach to recognize the biological framework of the pathology. “Understanding a complex disease such as AD is not just knowing about its present but also about its past. It is important to study the origin of the pathology and the biological limits leading us to it; only by knowing this information we will be able to plan the stages of a comprehensive clinical research”, he states.

In addition, concerning the next steps is this research area, the scientist points out that every hypothesis must be assessed “with quantifiable data and evidence”.

First of all, comparative neuroanatomy “should carefully assess the differences between human and non-human primates in parietal areas”. Secondly, we should evaluate “whether metabolic problems linked to AD are really born in structures and processes of our species”. Third, it is important to take into account “the physical causes of the metabolic defect, such as thermal, vascular, toxic and maintenance factors.” Finally, we have to determine “the process of a metabolic defect in some areas to produce a defect in other structures”.

“We already have many indications for all these stages but further experimental data are needed. As speculative proposal, we have to assess the possibility of finding bone markers associated with the disease, which would allow to study the disease in extinct hominids or in historical populations”, he adds.

Evolutionary Biology and Medicine

Emiliano Bruner works on digital anatomy and computerized morphometry. His research also includes studies on brain metabolism evolution and parietal areas evolution. This is not the first time the researcher takes part in joint studies on evolutionary biology and medicine, he has contributed in areas such as dementia, schizophrenia and myopia.

Nevertheless, this hypothesis “was born in my collaboration with Heidi Jacobs, an incredibly active and productive researcher in the field of neuropsychology”. Jacobs works at the Forschungszentrum Jülich (Germany) and at the Alzheimer Centrum Limburg (Netherlands), with research projects on dementia, neuron anatomy, brain metabolism, metabolic disorders, brain fitness, brain stimulation and biomarkers.