Similar calcification process in acute and chronic human brain pathologies

Abstract

Cellular microcalcification observed in a diversity of human pathologies, such as vascular dementia, Alzheimer's disease, Parkinson's disease, astrogliomas, and posttraumatic epilepsy, also develops in rodent experimental models of central nervous system (CNS) neurodegeneration. Central to the neurodegenerative process is the inability of neurons to regulate intracellular calcium levels properly, and this is extensible to fine regulation of the CNS. This study provides evidence of a common pattern of brain calcification taking place in several human pathologies, and in the rat with glutamate-derived CNS lesions, regarding the chemical composition, physical characteristics, and histological environment of the precipitates. Furthermore, a common physical mechanism of deposit formation through nucleation, lineal growth, and aggregation is presented, under the modulation of protein deposition and elemental composition factors. Insofar as calcium precipitation reduces activity signals at no energy expense, the presence in human and rodent cerebral brain lesions of a common pattern of calcification may reflect an imbalance between cellular signals of activity and energy availability for its execution. If this is true, this new step of calcium homeostasis can be viewed as a general cellular adaptative mechanism to reduce further brain damage.

Coaccumulation of Calcium and β-Amyloid in the Thalamus after Transient Middle Cerebral Artery Occlusion in Rats

“…Instead, a consistent finding was a calcium coaccumulation in the deposits. Previously, calcium precipitation has been observed in a number of acute and chronic brain diseases related to excitotoxic cell death and neurodegeneration (Rodriguez et al, 2000;Ramonet et al, 2006). Impaired calcium homeostasis has also been reported following focal cerebral ischemia (Shirotani et al, 1994;Watanabe et al, 1998).…”

Fahr’s disease: a rare diagnosis requiring admission to the emergency department

“…The incidence of basal ganglia calcification increases as the duration of hypocalcemia increases, with symptoms of calcification emerging after about 30 years [11]. Replacement of calcium and vitamin D improves metabolic abnormalities and delays clinical progression [12,13].…”

Pattern of Injury with a Graded Excitotoxic Insult and Ensuing Chronic Medial Septal Damage in the Rat Brain

“…Calcification develops in most areas of the rat brain following the in-vivo microinjection of several excitotoxins, and also develops in humans after acute brain injury (Ramonet et al, 2006;Casanova and Araque, 2003;Rodríguez et al, 2001;Herrmann et al, 1998;Ansari et al, 1990). The pattern of calcification in each area of the brain reflects its sensitivity to injury (Lammie et al, 2005;Rodríguez et al, 2004;Bernal et al, 2000;Mahy et al, 1995).…”