Common Supplements Combat Age-Related Memory Loss, Enhance Cognitive Performance
By Jim English
作者: Jim English
The human brain is one of the most elegant and complex structures ever conceived. Comprising over ten billion neurons and supportive cells, no other organized structure – organic or silicon – can begin to match the sheer complexity and processing power of the human brain. It regulates virtually all life systems while simultaneously generating the thoughts, dreams and feelings that define us and shape our perception of reality.
Every thought, concept, opinion, belief and emotion arises from the untold millions of chemical and electrical reactions that occur in the brain every second. And generating the power to drive all of this activity places a huge demand on the body’s energy reserves. Though it accounts for a mere two percent of body’s weight, the brain greedily consumes more than twenty percent of the body’s available energy in the form of oxygen and glucose.
The Aging Brain
By age seventy most people will have lost about ten percent of their original brain cells to the effects of “normal” aging. This continual loss of brain cells is further aggravated by damage from other age-related conditions, including hypertension, arteriosclerosis (hardening of the arteries), diabetes, and cerebrovascular diseases (CVD) such as cerebrovascular insufficiency, strokes and multi-infarct dementia (MID).
Dementia is defined as the loss of cognitive or intellectual functions. Unlike occasional forgetfulness, dementia is marked by a profound impairment of memory and the loss of complex abilities required for problem-solving, decision making, spatial orientation, and even the ability to put simple words together to communicate.
Dementia is a permanent, progressive disease that mostly affects the elderly, who, over time, may lose the ability to function normally and require round-the-clock care. It is estimated that up to 8 percent of all people over 65 suffer from some form of dementia, and these numbers double every additional five years, with an estimated 20 percent to 50 percent of people in their 80s suffering from some form of dementia.
痴呆症是一种永久性的进行性疾病，主要影响老年人，随着时间的推移，老年人可能会丧失正常生活能力，需要全天候的护理。据估计，高达8% 的65岁以上的人患有某种形式的痴呆症，这个数字每五年翻一番，估计有20% 到50% 的80多岁的人患有某种形式的痴呆症。
There are close to fifty different causes of dementia, including neurological disorders (Alzheimer’s disease), vascular disorders (multi-infarct disease), inherited disorders (Huntington’s disease), and infections (viruses such as HIV).
One factor shared by all of these disorders is a reduction in the flow of blood and oxygen to the brain. In addition to depriving brain cells of fuel, reduced circulation contributes to increased production of free radicals that inflict additional damage to cell membranes, further accelerating brain cell death. The continued loss of brain cells to the ravages of age and debilitating effects of degenerative diseases only speeds up the process of mental deterioration. As memories fade the ability to form new thoughts and solve problems is further reduced. Depression, incontinence, disorientation, speech disturbances, tremor, muscle weakness, tinnitus (ringing in the ears), and loss of both visual acuity and coordination also worsen as these conditions progress.
Alzheimer’s disease (or “senile dementia of the Alzheimer type”) is a chronic and progressive degenerative neurological condition that afflicts over four million people in the United States, accounting for up to 60 percent of all cases of dementia. Alzheimer’s commonly appears after age fifty, and from age sixty-five on, the risk of developing the disease doubles with every additional five years of age. As if these numbers weren’t bad enough, they are expected to increase in the coming decades, draining health care resources, and leaving almost no family untouched.
Aging adults face loss of cognitive powers and mental functions. Research supports the role of a number of potent anti-aging therapies to slow brain aging and preserve cognitive function. 老年人面临认知能力和精神功能的丧失。研究支持了一些有效的抗衰老疗法在延缓大脑衰老和保持认知功能方面的作用
While there is currently no cure for Alzheimer’s, ongoing research shows that several nutrients may help to halt the destructive progression of dementia and improve cognitive function of patients suffering from Alzheimer’s and other forms of dementia.
Hope for Aging Brains
While medical researchers and pharmaceutical companies race to patent new (and profitable) treatments for Alzheimer’s and other degenerative brain conditions, a number of existing nutritional compounds have already been proven to safely support healthy brain function while protecting and prolonging cognitive ability. Supported by numerous double-blind controlled trials in Europe and the U.S., these supplements can slow down the age-related loss of higher-level cognitive functions that can appear in healthy individuals as young as fifty years of age.
Acetyl-L-Carnitine (ALC) is a cognitive enhancer and neuroprotective agent that protects against a wide range of age-related degenerative changes in the brain and nervous system. ALC is an ester of carnitine that modulates cellular concentrations of free coenzyme A and acetyl-coenzyme A, two compounds integrally involved in numerous cellular functions, including the transfer of fatty acids across mitochondrial membranes for energy production.
乙酰肉碱是一种认知增强剂和神经保护剂，可以保护大脑和神经系统免受与年龄相关的退化性变化的影响。ALC 是一种肉碱酯，可以调节细胞内游离辅酶 a 和乙酰辅酶 a 的浓度，这两种化合物整体参与多种细胞功能，包括通过线粒体膜转移脂肪酸以产生能量。
ALC is found in various concentrations in the brain and its levels are significantly reduced with aging. ALC also significantly reduces damaged fats, such as lipofuscin, in the brains of aged rats. In addition to accumulating in the aging brain, lipofuscin also accumulates in the skin as “aging spots,” those brownish pigmented blemishes that accumulate in the backs of hands of many people over fifty. The reduction of these deposits following consumption of ALC may be evidence of a slowing in the aging process in the brain.
ALC 存在于大脑中的不同浓度中，随着年龄的增长，其水平显著降低。ALC 还显著减少老年大鼠大脑中受损的脂肪，如脂褐素。除了在老化的大脑中积累，脂褐素还在皮肤上积累成为“老化斑点” ，这些褐色色素斑点积累在许多五十岁以上的人的手背上。消耗 ALC 后这些沉积物的减少可能是大脑衰老过程减缓的证据。
ALC also has the ability to cross into the brain where it acts as a powerful antioxidant, preventing the deterioration of brain cells that normally occurs with age. ALC 还具有进入大脑的能力，在大脑中充当一种强大的抗氧化剂，防止随着年龄增长而出现的脑细胞退化
ALC also has the ability to cross into the brain where it acts as a powerful antioxidant, preventing the deterioration of brain cells that normally occurs with age. Because of this protective effect, ALC may be beneficial in the prevention and treatment of free-radical mediated diseases, such as Alzheimer’s and Parkinson’s disease.
ALC 还具有进入大脑的能力，在大脑中充当一种强大的抗氧化剂，防止随着年龄增长而出现的脑细胞退化。由于这种保护作用，ALC 可能有利于预防和治疗自由基介导的疾病，如阿尔茨海默氏症和帕金森氏症。
Alzheimer’s disease primarily affects cholinergic function. ALC has been shown to promote both the release and synthesis of acetylcholine. Additionally, ALC promotes high affinity uptake of choline, which declines significantly with age.
阿尔茨海默病主要影响胆碱能功能。ALC 已被证明能促进乙酰胆碱的释放和合成。此外，ALC 促进高亲和力的胆碱吸收，而胆碱吸收随着年龄的增长而显著下降。
In addition to ALC’s cholinergic-enhancing properties, researchers have shown that ALC has numerous beneficial effects on dopaminergic neurons. The decline of the dopaminergic neurotransmission system is most evident in Parkinson’s disease patients.
除了 ALC 的胆碱能增强特性之外，研究人员还发现 ALC 对多巴胺能神经元有许多有益的作用。在帕金森病患者中，多巴胺能神经传导系统的衰退最为明显。
ALC has been shown to improve age-related changes of dopamine receptors, including improved release and binding of dopamine. Research has shown that ALC can prevent dopaminergic neuron death caused by MPTP, a neurotoxin that mimics neurological symptoms similar to Parkinson’s disease, by selectively killing dopaminergic neurons.
ALC 已被证明可以改善多巴胺受体与年龄相关的变化，包括改善多巴胺的释放和结合。研究表明 ALC 可以选择性杀死多巴胺能神经元，从而防止 MPTP 引起的多巴胺能神经元死亡。
Choline is a precursor to acetylcholine, a cholinergic neurotransmitter that declines with advancing age. Individuals predisposed to Alzheimer’s disease and other dementias, infants and children, diabetics, and athletes (who often have reduced plasma-choline levels after training or competition) may be at increased risk of choline deficiency.
Choline has been shown to have considerable potential for preserving the integrity of neuronal structures and in preventing some of the alterations in the central nervous system during aging. Choline supplementation appears to prevent the age-induced decline of the dendritic network composed of neurons that fire impulses to the cells. Choline increases the number of dendritic spines in the cerebral cortex of old mice and improves the animals’ learning performance.
Under conditions of increased demand for acetylcholine production, excess choline availability becomes a limiting factor for acetylcholine synthesis. When this additional exogenous choline supply is unavailable, cholinergic neurons are able to use free choline taken from a choline “reservoir” to continue the synthesis of acetylcholine.
This process, termed “autocannibalism,” can lead to a decrease in the quantity and quality of membrane in these cells. Indeed, cholinergic neurons’ ability to use this alternative source of choline appears to contribute to their vulnerability in Alzheimer’s disease.
Researchers believe defects in choline-metabolism may play a central role in the development of Alzheimer’s disease as defects in choline transport exist in the cells of Alzheimer’s victims. Defects in choline metabolism may also be influential in Down’s syndrome, normal aging, Huntington’s disease, amyotropic lateral sclerosis, the familial dysautonomias, and the post-polio syndrome.
DMAE (dimethylaminoethanol) is a nutrient found abundantly in fish and in human brains. In the brain, DMAE is converted into choline, the precursor to acetylcholine. Because acetylcholine conducts nerve impulses within the brain, the increased acetylcholine synthesis seen after DMAE supplementation may improve memory and learning skills, elevate mood, prevent memory loss in elderly adults, and increase physical energy.
DMAE (二甲基乙醇胺)是一种在鱼类和人类大脑中大量发现的营养素。在大脑中，DMAE 被转化为胆碱，乙酰胆碱的前体。由于乙酰胆碱在大脑中传导神经冲动，DMAE 补充剂后增加的乙酰胆碱合成可以改善记忆和学习技能，提升情绪，防止老年人的记忆丧失，增加体力。
Studies suggest DMAE may work by inhibiting choline metabolism in peripheral tissues, causing free choline to accumulate in the blood, enter the brain and stimulate choline receptors. As the immediate precursor to choline, DMAE assists in the building and repair of cell membranes, particularly in the brain and central nervous system.
研究表明，DMAE 可能通过抑制外周组织的胆碱代谢，导致游离胆碱在血液中积累，进入大脑并刺激胆碱受体而发挥作用。作为胆碱的直接前体，DMAE 协助细胞膜的建立和修复，特别是在大脑和中枢神经系统。
As the immediate precursor to choline, DMAE assists in the building and repair of cell membranes, particularly in the brain and central nervous system. 作为胆碱的直接前体，DMAE 协助细胞膜的建立和修复，特别是在大脑和中枢神经系统
Animal studies have demonstrated that DMAE stimulates brain neurons and improves working memory performance. In one study, rats treated with DMAE demonstrated significant improvements in remembering how to negotiate a maze. In another study, mice trained to negotiate a maze demonstrated improved memory retention when treated with DMAE.
动物研究表明，DMAE 刺激大脑神经元，提高工作记忆的表现。在一项研究中，用 DMAE 处理过的老鼠在记忆如何走迷宫方面表现出显著的改善。在另一项研究中，经过走迷宫训练的老鼠在接受 DMAE 治疗后，记忆力得到了改善。
DMAE’s ability to stimulate acetylcholine synthesis has led researchers to explore its effects in senile dementia and Alzheimer’s. In a promising study, 14 senile dementia patients were treated with DMAE for four weeks. The dosage was gradually increased to 600 mg, three times daily, during the first two weeks, with no adverse effects. Although the patients experienced no improvement in cognitive function or memory, ten of the 14 patients experienced reduced depression, irritability and anxiety and increased motivation and initiative.
DMAE 刺激乙酰胆碱合成的能力已经引导研究人员探索其在老年痴呆症和阿尔茨海默氏症中的作用。在一项有前景的研究中，14名老年痴呆症患者接受 DMAE 治疗4周。在最初的两周内，剂量逐渐增加到600毫克，每日三次，没有不良反应。尽管患者的认知功能和记忆力没有改善，但14名患者中有10名患者的抑郁、易怒和焦虑症状减轻，动力和主动性增强。
Phosphatidylserine (PS) is a naturally-occurring phospholipid nutrient that has been shown to improve cognitive functions and enhance mental ability. PS is essential to the healthy functioning of the human brain where it affects an assortment of nerve cell functions, including: conduction of nerve impulses; accumulation, storage and release of neurotransmitters; the activity and number of receptors involved in synaptic discharge; and the biological maintenance of cellular ‘housekeeping’ functions.
磷脂丝氨酸是一种天然磷脂营养素，已被证明可以改善认知功能和提高心理能力。PS 对人类大脑的健康功能至关重要，它影响神经细胞功能的分类，包括: 神经冲动的传导; 神经递质的积累、储存和释放; 参与突触放电的受体的活性和数量; 以及细胞内务功能的生物维持。
Supplementation with PS has been proven to slow, halt, or in many cases, even reverse cognitive degeneration due to Age-Related Cognitive Decline (ARCD), and dementing illnesses like Alzheimer’s disease.
补充 PS 已经被证明可以减缓、阻止甚至在许多情况下逆转由于年龄相关的认知衰退(ARCD)引起的认知退化，以及像阿尔茨海默氏症这样的疾病。
Phosphatidlyserine has been scientifically established to be among the most effective substances to consistently result in dramatic cognitive improvements and enhancements of other higher brain functions.
PS is extremely bioavailable and crosses the blood-brain barrier with ease. Once in the brain, the PS molecule as a unit merges smoothly into the nerve cell membrane where it is available to facilitate cell-level energy and homeostasis, as well as enhance neurotransmitter production, release, and action. PS also serves as a precursor reservoir for the related phospholipids, phosphatidylethanolamine and phosphatidylcholine.
PS 具有极强的生物可利用性，可以轻松地跨越血脑屏障。一旦进入大脑，PS 分子作为一个整体顺利地融入神经细胞膜，在那里它可以促进细胞水平的能量和稳态，以及增强神经递质的产生、释放和行动。聚苯乙烯还是相关磷脂、磷脂酰乙醇胺和磷脂酰胆碱的前体储存库。
Findings from many controlled clinical trials indicate that PS consistently ameliorates memory loss and other cognitive decline related to aging. In 14 double-blind clinical trials, conducted with subjects aged 50 and older, PS benefited all degrees of cognitive impairment. In one trial subjects with age-related cognitive decline (ARCD), PS reversed the decline of name-face acquisition skills by a statistical 12 years; i.e., from average scores attained by 64-year-old subjects to average scores attained by 52-year-olds. As the investigators noted, it’s as if they had “rolled back the clock” measuring “cognitive biological age” by roughly 12 years, in terms of overall cognitive status.
许多对照临床试验的结果表明，PS 能持续改善与年龄有关的记忆丧失和其他认知衰退。在14个双盲临床试验中，受试者年龄在50岁以上，PS 受益于所有程度的认知障碍。在一个与年龄相关的认知能力下降(ARCD)的试验对象中，PS 通过12年的统计逆转了名字-面孔习得技能的下降，即从64岁受试者的平均分到52岁受试者的平均分。正如研究人员指出的那样，就整体认知状态而言，这就好像他们把“认知生物学年龄”的测量“倒退了大约12年”。
Findings from many controlled clinical trials indicate that PS consistently ameliorates memory loss and other cognitive decline related to aging. 许多对照临床试验的结果表明，PS 能持续改善与年龄有关的记忆丧失和其他认知衰退
In double-blind trials conducted with more severely afflicted subjects, PS brought about statistically and clinically significant improvements in measures of recall, learning, concentration, adaptability, mood and sociability. In other double-blind trials, PS improved neuro-physiological measures such as EEG (electroencephalogram) and reflexes (as judged by flicker-fusion response time).
在对更严重的患者进行的双盲试验中，PS 在记忆力、学习能力、注意力、适应能力、情绪和社交能力的测量方面带来了统计学和临床上的显著改善。在其他双盲试验中，PS 改善了神经生理测量，如 EEG (脑电图)和条件反射(根据闪烁融合反应时间判断)。
In another trial conducted with young male volunteers, PS significantly improved EEG alpha rhythm (which often declines with age and memory loss). In older subjects with severe cognitive impairment, PS dramatically enhanced brain glucose consumption (assessed via positron emission tomographic [PET] imaging) and partially restored the 24-hour rhythm of TSH (thyroid-stimulating hormone) secretion in aged men. Also, in elderly subjects, PS enhanced the hypothalamic-pituitary-adrenal (HPA) stress-coping axis, as assessed by the dexamethasone suppression test.
在另一项对年轻男性志愿者进行的试验中，PS 显著改善了 EEG alpha 节律(通常随着年龄和记忆力的丧失而下降)。在有严重认知障碍的老年受试者中，PS 显著提高了大脑葡萄糖消耗(通过正电子发射断层摄影[ PET ]成像评估) ，部分恢复了老年男性24小时 TSH (促甲状腺激素)分泌的节律。此外，在老年受试者，PS 增强了下丘脑-垂体-肾上腺(HPA)应激应对轴，由地塞米松抑制试验评估。
A number of clinical studies have shown that Ginkgo biloba can protect brain cells from damage caused by free radicals while improving blood circulation and oxygen delivery, particularly through the microcapillaries. In one study, researchers measured a fifty-seven percent increase in blood flow through capillaries within sixty minutes of giving Ginkgo to volunteers.
A second study by German scientists involved 60 patients diagnosed with cerebral insufficiency and depression. Patients receiving Ginkgo extract began to show marked improvement after only two weeks, with a significant reduction of many of their symptoms.
In another clinical trial of 166 patients over the age of sixty, researchers found that patients suffering from cerebral insufficiency showed a significant improvement following three months of treatment, confirming the efficacy of Ginkgo extract in cerebral disorders due to aging.
Researchers have also found that Ginkgo can be especially helpful when given to Alzheimer’s patients at the first sign of symptoms. In one published study, German scientists gave a daily dose of 120 mg of Ginkgo to twenty elderly patients exhibiting various early symptoms of dementia. The results were dramatic, and the patients receiving Ginkgo showed impressive improvements on a variety of clinical tests, as compared to patients receiving a placebo.
In one large study published in 1996, German researchers tested Ginkgo extract on a group of 222 patients, aged fifty-five or older, who were diagnosed with mild to moderate dementia caused by either Alzheimer’s disease or multi-infarct dementia. Patients were given either 240 milligrams of Ginkgo biloba extract, twice a day before meals, or a placebo, for the duration of the six-month long trial.
At the conclusion of the study the researchers reported that patients receiving Ginkgo showed a remarkable overall improvement in their condition, including a 300 percent increase in memory and attention as compared to those receiving the placebo pills.
The researchers concluded their report by stating that, in cases of dementia, Ginkgo extract could improve a patient’s quality of life while preserving independence and postponing the need (and expense) of full-time care.
Ginkgo and Multi-Infarct Dementia
The second most common cause of dementia in older people is multi-infarct dementia (MID), a condition that accounts for about fifteen percent of all cases of dementia. Multi-infarct dementia usually affects people between the ages of 60 and 75, and men are more likely to have multi-infarct dementia than women. MID is typically caused by a series of mini-strokes, also referred to as transient ischemic attacks (TIAs), that can occur when an artery in the brain either becomes blocked or ruptures. Strokes are generally caused by high blood pressure, high blood cholesterol, diabetes, and heart disease. Of these causes, the most important risk factor for multi-infarct dementia is untreated high blood pressure. In fact, it is extremely rare for a person to develop multi-infarct dementia without also having high blood pressure.
老年人痴呆症的第二大常见原因是血管性痴呆，这种疾病约占所有痴呆症病例的15% 。血管性痴呆通常影响60到75岁的人群，男性比女性更容易患血管性痴呆。MID 通常是由一系列的小中风引起的，也被称为短暂性脑缺血发作(tia) ，这种发作可能发生在大脑动脉阻塞或破裂时。中风通常由高血压、高血胆固醇、糖尿病和心脏病引起。在这些原因中，血管性痴呆最重要的危险因素是未经治疗的高血压。事实上，对于一个人来说，没有高血压的情况下患上血管性痴呆是极其罕见的。
While these mini-strokes may or may not be noticed at the time, the effect on the brain is the same – brain cells become damaged by a lack of oxygen and die. Over time a series of mini-strokes can begin to destroy substantial portions of the brain that control speech and visual processing.
As with Alzheimer’s disease, Ginkgo has been shown to help patients suffering from MID by enhancing memory, alertness and overall quality of life. Additionally, given the underlying disorders that cause blood vessels to rupture, Ginkgo can also benefit patients suffering from MID by restoring elasticity and strength to stiff, weakened blood vessels.
与阿尔茨海默病一样，银杏已被证明可以通过提高记忆力、警觉性和整体生活质量来帮助 MID 患者。此外，考虑到导致血管破裂的潜在疾病，银杏还可以通过恢复坚硬、虚弱的血管的弹性和强度，使 MID 患者受益。
Baby boomers and aging adults face a loss of cognitive powers and impaired mental functions. Research supports the role of a number of potent anti-aging therapies to slow brain aging and preserve cognitive function. Rather than waiting for signs of an irreversible decline in mental abilities or other more serious cognitive problems, it would be prudent to take steps to support the brain’s ability to heal and self-repair. In short, we can take steps now to slow age-dependent brain cell changes, preserve vital functions, and maintain mental health and vigor.