Blood sugar dysregulation damages learning and memory

Posted on November 24, 2010 by Dr. Jonathan

More evidence for the deleterious effects on the brain of hyperglycemia and hypoglycemia is presented in a study just published in the journal Biochimica et Biophysica Acta (BBA) – Molecular Basis of Disease. The authors’ research was designed to…

“…evaluate the effects of streptozotocin (STZ)-induced hyperglycemia and insulin-induced hypoglycemia in cortical and hippocampal mitochondria bioenergetics and oxidative status.”

The hippocampus is the seat of short-term memory and a regulatory center for adrenal function. STZ-induced hyperglycemia and insulin-induced hypoglycemia are standard methods employed to examine the physiological repercussions of high and low blood sugar respectively. They analyzed the respiratory chain and phosphorylation system for the capacity to produce energy in the mitochondria (cellular energy ‘factories’), thiobarbituric acid reactive substances (TBARS) levels and the hydrogen peroxide (H2O2) production rate for oxidative stress, and non-enzymatic and enzymatic antioxidant defenses. What did their data show?

“Cortical mitochondria from insulin-induced hypoglycemic rats present a significant decrease in the ADP/O index, a significant increase in the repolarization lag phase and a decrease in GSH/GSSG ratio when compared with STZ and control mitochondria. Both STZ-induced diabetes and insulin-induced hypoglycemia promote a significant increase in TBARS levels and a decrease in glutathione disulfide reductase activity. Diabetic cortical mitochondria present a significant decrease in glutathione peroxidase (GPx) activity compared to control mitochondria. In turn, insulin-induced hypoglycemia induced a significant increase in GPx and manganese superoxide dismutase (MnSOD) activities. In hippocampal mitochondria, insulin-induced hypoglycemia increases the respiratory control ratio whereas both situations, hyper- and hypoglycemia, potentiate H2O2 production and decrease the activity of MnSOD.”

In other words, both hyper- and hypoglycemia impair cortical and hippocampal function deranging energy production, increasing damage due to oxidative stress. In reference to type 1 diabetes, the authors state in conclusion:

“These results suggest that the poor glycemic control that occurs in type 1 diabetic patients undergoing insulin therapy may have detrimental effects in brain areas involved in learning and memory.”

Mild memory loss is neuropathology, not ‘normal aging’

Posted on September 24, 2010 by Dr. Jonathan

There is an erroneous popular notion that mild memory lapses, so-called ‘senior moments’, are a normal consequence of aging. A study just published in the journal Neurology introduces more evidence that age-related memory decline does not occur in the absence of the same kind of neuropathologic brain lesions associated with full-blown dementia. The authors’ intention was…

“To assess the contribution of dementia-related neuropathologic lesions to age-related and disease-related change in cognitive function.”

They examined 354 subjects for up to 13 years with annual clinical evaluations including detailed tests of cognitive function. At death their brains underwent autopsy and were examined for neuropathologies including neurofibrillary tangles, Lewy bodies and cerebral infarct (evidence of stroke)—the same pathologies known to be associated with dementia. Their data offers strong encouragement to learn how to take care of your brain:

“During follow-up, rate of global cognitive decline was gradual at first and then more than quadrupled in the last 4 to 5 years of life consistent with the onset of progressive dementia. Neurofibrillary tangles, cerebral infarction, and neocortical Lewy bodies all contributed to gradual age-related cognitive decline and little age-related decline was evident in the absence of these lesions. Neurofibrillary tangles and neocortical Lewy bodies contributed to precipitous disease-related cognitive decline, but substantial disease-related decline was evident even in the absence of these lesions.”

In other words, not everyone experiences memory decline with age. When it does occur, it is due to the same damage to brain tissue that can evolve into dementia. As the authors state in their conclusion:

“Mild age-related decline in cognitive function is mainly due to the neuropathologic lesions traditionally associated with dementia.“

See earlier and forthcoming posts in the Brain Health category for more science on how to take care of your brain.

Magnesium enhances learning and memory

Posted on March 12, 2010 by Dr. Jonathan

Neuron As the authors of this paper recently published in the journal Neuron state:

“Learning and memory are fundamental brain functions affected by dietary and environmental factors.” The authors “show that increasing brain magnesium…leads to the enhancement of learning abilities, working memory, and short- and long-term memory…”

Facilitation (the pathways become more efficient) and long-term potentiation (the synapses become more efficient) are the means by which learning and memory are ‘sculpted’ in the brain. The authors go on to conclude:

“Our findings suggest that an increase in brain magnesium enhances both short-term synaptic facilitation and long-term potentiation and improves learning and memory functions.”

Though they used a novel form, it’s the magnesium in the brain, not the form, that does the job. This is another item added to the long list of reasons to keep your magnesium up. The next time you suffer a leg or foot cramp remember—this may be affecting your brain too.