Interactions between neurons and glia
Motor and Sensitive Neurons
Sensitive Nerves Map
Cutaneous Fields of Peripheral Nerves
Morelli: How ATP is synthesized in Neurons?
Glutamine 0.4-0.75 mM
Glucose 5 mM
both freely permeable to nerves
glutamine--> glutamate + NH3
alpha ketoglutarate + alanine --> glutamate + pyruvate
Homocysteine, vitamin B6, and vascular disease in AD patients. 2002. 2002 May 28;58(10):1471-5. Neurology. 2002 May 28;58(10):1471-5.
Miller JW, Green R, Mungas DM, Reed BR, Jagust WJ.
Department of Medical Pathology, University of California, Davis, School of Medicine, Sacramento 95817, USA. email@example.com
Cerebrovascular disease is a cause of dementia and is associated with elevated plasma levels of homocysteine. Patients with AD tend to have unexplained elevations of homocysteine concentrations vs healthy control subjects. Vitamin B(6) status, a potential determinant of plasma homocysteine, has not been characterized in patients with AD.
To investigate plasma homocysteine, vitamin B(6) status, and the occurrence of vascular disease in patients with AD.
Forty-three patients with AD and 37 control subjects without AD were studied for homocysteine, B vitamin status (folate, vitamin B(12), pyridoxal-5'-phosphate [PLP]), kidney function (creatinine), and thyroid function (thyroid-stimulating hormone, thyroxin). In addition, the presence of vascular disease was assessed by reviewing both medical histories and brain imaging data provided by CT and MRI.
The OR for elevated plasma homocysteine (>12 micromol/L) was only 2.2 (not significant) for subjects with AD. In contrast, the OR was 10.0 (p = 0.03) for subjects with vascular disease (n = 26). The OR for low plasma PLP (<25 nmol/L) was 12.3 (p = 0.01) for patients with AD. No significant relationship was observed between vascular disease and PLP level or between plasma homocysteine and PLP concentrations.
Elevated plasma homocysteine in patients with AD appears related to vascular disease and not AD pathology. In addition, low vitamin B(6) status is prevalent in patients with AD. It remains to be determined if elevated plasma homocysteine or low vitamin B(6) status directly influences AD pathogenesis or progression.
Proc Natl Acad Sci U S A. 2010 Oct 12;107(41):17763-7. Epub 2010 Sep 13.
Spatial correlation between brain aerobic glycolysis and amyloid-β (Aβ ) deposition.
Vlassenko AG, Vaishnavi SN, Couture L, Sacco D, Shannon BJ, Mach RH, Morris JC, Raichle ME, Mintun MA.
Department of Radiology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Amyloid-β (Aβ) plaque deposition can precede the clinical manifestations of dementia of the Alzheimer type (DAT) by many years and can be associated with changes in brain metabolism. Both the Aβ plaque deposition and the changes in metabolism appear to be concentrated in the brain's default-mode network. In contrast to prior studies of brain metabolism which viewed brain metabolism from a unitary perspective that equated glucose utilization with oxygen consumption, we here report on regional glucose use apart from that entering oxidative phosphorylation (so-called "aerobic glycolysis"). Using PET, we found that the spatial distribution of aerobic glycolysis in normal young adults correlates spatially with Aβ deposition in individuals with DAT and cognitively normal participants with elevated Aβ, suggesting a possible link between regional aerobic glycolysis in young adulthood and later development of Alzheimer pathology.
Defective organellar acidification as a cause of cystic fibrosis lung disease: reexamination of a recurring hypothesis 2009