In his 1932 inaugural address, FDR told the world that we have nothing to fear but fear itself. If you ask people today what they fear, the list will likely include more specific things, like public speaking, ostracism, blindness, death, poverty, failure, memory loss, disease and a host of other states, conditions or activities. Some fears can be overcome with counseling, such as acrophobia; some can be prevented by being active instead of passive, such as poverty and failure; and some might require nutritional or medical intervention, such as certain diseases. Getting and using education, which doesn’t necessarily entail sitting in a classroom, might possibly attend to these needs. A modern-day fear is that of Alzheimer’s disease (AD), one that people associate with memory dysfunction, disorientation, and eventual loss of function. It’s a matter of not knowing that you don’t know. And it’s frightening.

The loss of cognitive ability takes a while to manifest, maybe ten to fifteen years, and is associated with the development of abnormal tissues and protein deposits in the brain’s cerebral cortex, which is the outermost layer of gray matter responsible for higher brain functions, such as sensation, voluntary muscle movement, thought, reasoning and memory. The primary neurotransmitter involved with the latter three of these cerebral obligations is acetylcholine, which is released at the ends of nerve fibers to send nerve impulses from one cell to another. Other jobs of this neurotransmitter involve decreasing heart rate and contraction strength, dilating blood vessels, increasing peristalsis, and raising elimination pressure during urination.

The dementia we fear results in deterioration of mental faculties, causing apathy, confusion and occasional stupor. A couple centuries ago it was synonymous with insanity, and was termed dementia praecox, now known as schizophrenia. Of its several forms, senile dementia is the one most commonly recognized, usually occurring after age 65, though it can happen earlier.

Natural deficits of acetylcholine accompany the aging process, causing those sporadic lapses in short-term memory that many individuals experience from time to time. Called benign forgetfulness, this non-debilitating memory decline is not to be confused with Alzheimer’s disease. It’s the degeneration of neurons in the cerebral cortex that leads to difficulties with language and judgment in AD. From the cortex, degeneration proceeds to the hippocampus, which is the part of the limbic system that deals with memory and spatial navigation. The hippocampus helps us to retain facts that pertain to specific events so they can be regurgitated if needed, but it also helps to order the chronology of one’s lifetime events. All this is what we typically call recollection. Memory tasks usually excite considerable hippocampus engagement, but that response is substantially weakened by advancing age, particularly in the absence of nutrients that feed the process. In transient global amnesia, a state induced by statin drugs’ cholesterol reduction and subsequent interference with the body’s manufacture and use of co-enzyme Q10, hippocampus activity is seriously constrained, though reversible by judicious supplementation of the enzyme.

Late in the last century, scientists demonstrated interest in the enhancement of memory in lab animals by introducing the phospholipid called phosphatidylcholine (PC) to their diets. “Demented” mice showed very low levels of choline and acetylcholine. After adding PC to the rations of the experimental group, the examiners saw an expected reversal in choline and acetylcholine levels, and an improvement in memory (Chung, 1995). Yes, mice are not the same as people, but they share a commonality in cerebral function, providing a good model for this scrutiny of memory acquisition and retention (Moriyama, 1996).

PC not only increases neurotransmitter efficiency, but also improves the supportive nature of polyunsaturated fatty acids (PUFA’s) in the revival of cell membrane fluidity. Since PC is the major structural and functional component of the cell membrane, this is not small news. Its reinstatement to a place of high stature in membrane architecture helps to sequester renegade substances that inhibit the membrane’s full capabilities in directing the machinery of life (Hiratsuke, 2009) (Gong, 2004).

After it was found that Alzheimer’s disease is related to abnormal metabolism of membrane phospholipids, researchers began to examine faulty homeostasis for discovery of diagnostic biomarkers. Alterations in phosphatidylcholine and phosphatidylethanolamine values were seen as indicative of membrane breakdown that could lead to fatty acid and phospholipid-related disorders that include dementias (Gonzalez-Dominguez, 2014). This is of particular interest because the pathophysiological changes associated with AD begin decades before clinical symptoms appear (Trushina,2013) (Whiley, 2014).

Since the brain is about sixty percent fat, it seems logical to ensure its repletion. Fatty acids and phospholipids (PL’s) are the most crucial molecules to occupy the space. It’s not very likely that seniors can get sufficient phospholipids from their diets because of diminished sense of taste for food, living and eating alone, being food insecure, and being broke. We realize this doesn’t describe all people in the group, but it probably covers someone you know. Egg yolks, liver, wheat germ and peanuts have some of the precursors to PL’s, but frequency of ingestion and concentration are often insufficient. Neither are many older folks amply hydrated to allow the PL’s to become organized into carriers of helpful molecules. The administration of PL’s, notably PC, can do much to restore function—and structure—of the membranes that make life more enjoyably livable.

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