TY  - JOUR
AU  - Brenner, Steven R.
PY  - 2019
DA  - 2019/02/26
TI  - Sporadic Alzheimer Disease and That Developing in Down’s Syndrome: The Immune System Attacking Self Rather Than Suppressing Infectious Disease Invaders, Toll Like Receptors Triggering Excessive Cytosolic Calcium, Excess Calcineurin Activation, Overexpression of Regulator of Calcineurin1, Runaway Beta-Amyloid Production, Synaptic Loss, Destructive Inflammation and Dementia
JO  - OBM Geriatrics
SP  - 035
VL  - 03
IS  - 01
AB  - Alzheimer Disease may result from excessive stimulation of the innate immune system from development of underlying opportunistic infections and impaired age related self recognition as non-self, due to immunodeficiency and immunosenescence, resulting in excessive inflammation and runaway Beta-amyloid production (a component of the innate immune system) causing cytosolic calcium overload.  Excessive cytosolic calcium may cause over activation of calcineurin and inactivation of cis-trans prolyl isomerase (Pin1), with subsequent loss of dendritic spine maintenance, and synaptic destruction. 
Improving immune function, identifying and treating infections, avoiding runaway Beta-amyloid production and inhibiting calcineurin in a manner similar to that utilized in preventing tissue transplant rejection, may lead to improved prevention and treatment of Alzheimer Disease.
SN  - 2638-1311
UR  - https://doi.org/10.21926/obm.geriatr.1901035
DO  - 10.21926/obm.geriatr.1901035
ID  - Brenner2019
ER  -