Journal of Clinical & Experimental Neuroimmunology
Open Access

Brain atrophy affects loss of neurons. Some degree of atrophy and subsequent brain shrinkage is normal with old age, even in people who are cognitively healthy. However, atrophy is accelerated in individuals with mild cognitive impairment, even faster in those who eventually progress from mild cognitive impairment to Alzheimer’s. Many elements have concerned in affecting rate of brain atrophy, one of which is high levels of an amino acid in blood called homocysteine. Studies have display that hiked levels of homocysteine increase risk of Alzheimer’s.

In fresh randomised controlled trial, researchers investigated part of vitamin B in regulating levels of homocysteine. They particularly wanted to test whether lowering homocysteine through giving high doses of vitamin B for two years could reduce rate of brain atrophy in people with pre existing mild cognitive impairment. Volunteers aged seventy and older with concerns about their memory were listed for study. It was cleared that volunteers shall diagnosis of mild cognitive impairment, explained using specific criteria. These included a concern about memory that did not involve with activities of daily living, pre specified scores on some cognitive scales assessing word recall, fluency. Study prevented individuals with diagnosis of dementia, who were taking anti-dementia drugs or who had active cancer. Individuals taking folic acid and vitamin B6 or B12 above certain doses were prevented.

Both healthy, pathological brain aging are characterized by many degrees of cognitive lessen that strongly correlate with morphological changes adverted to as cerebral atrophy. These hallmark morphological alterations include cortical thinning, white, gray matter volume loss, ventricular enlargement, and loss of gyrification all caused by a myriad of subcellular, cellular aging procedures. While biology of brain aging has been investigated extensively, mechanics of brain aging still immensly understudied. Here, we advise a multiphysics model that couples tissue atrophy, Alzheimer’s disease biomarker progression. We take on multiplicative dispurse of deformation gradient into a shrinking and an elastic part. We model atrophy as region specific isotropic shrinking, separate between a constant, tissue dependent atrophy rate in healthy aging, an atrophy rate in Alzheimer’s disorder that is proportional to local biomarker concentration. Our finite element modeling approach delivers a computational framework to systematically study spatiotemporal progression of cerebral atrophy, its regional reault on brain shape. We regulate our results via comparison with cross sectional medical imaging studies that disclose persistent age related atrophy patterns. Our long term goal is to develop a diagnostic tool able to differentiate between healthy, accelerated aging, typically determined in Alzheimer’s and related dementias, in order to permit for earlier and more effective interventions.

Brain shape undergoes many changes throughout life. Advanced aging is characterized by progressive atrophy which seems brain volume loss, cortical thinning, sulcal widening, and ventricular enlargement. These morphological changes are part of healthy brain aging it still unclear how these changes relevant to cognitive decline. In case of accelerated aging, such in neurodegenerative diseases like AD, these structural changes are worse due to presence of neurotoxic proteins that spread through brain.