Acupuncture Continuing Education

Acupuncture Reduces Alzheimer’s Disease Brain Plaques

Acupuncture reverses brain damage caused by Alzheimer’s Disease plaques and improves memory. Researchers identified the ability of electroacupuncture to reduce pathological plaques in the brain caused by Alzheimer’s Disease. Furthermore, important biochemical secretions are regulated by electroacupuncture that correlate to benefits in cognitive functioning. Laboratory tests confirm that electroacupuncture causes improvements in cognitive functioning, brain plaque reduction, and restores regulation of brain neurotrophin growth factors. We’ll take a look at the acupuncture study’s results and also review important aspects of Alzheimer’s Disease pathology.


Scalp Acupoints


Researchers at The Fujian University of Traditional Chinese Medicine have made promising discoveries about the pathogenesis of Alzheimer’s Disease (AD) and have identified that electroacupuncture (EA) at the acupoint Baihui (DU20) may reverse key neurogenic factors of the disease. The study, conducted on mice, showed that electroacupuncture decreases cognitive impairment and deposits of β-amyloid (Aβ) — the plaque that is one of the defining signs of Alzheimer’s Disease. The researchers also found that electroacupuncture increases the ratio among brain-derived neurotrophic factors (BDNF) to favor those that promote neural potentiation over those that cause apoptosis (programmed cell death). Since ancient times, DU20 has been used to improve cognitive functioning but the mechanisms of action have only recently been mapped by scientific investigations. This study demonstrates that DU20 benefits cognitive functioning and also elucidates the mechanisms of action of the acupoint. 

According to the US Department of Health and Human Services, “dementia is the loss of cognitive functioning — thinking, remembering, and reasoning — and behavioral abilities to such an extent that it interferes with a person’s daily life and activities,” [1] and Alzheimer’s Disease is the most common cause of dementia in aged people. Although the disease is commonly understood as a progressive loss of memory, it likely begins years before any cognitive symptoms appear. “Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain, and once-healthy neurons stop functioning, lose connections with other neurons, and die. The damage initially appears to take place in the hippocampus, the part of the brain essential in forming memories. As more neurons die, additional parts of the brain are affected, and they begin to shrink. By the final stage of Alzheimer’s, damage is widespread, and brain volume has shrunk significantly.” [2]

The progressive cognitive deterioration in Alzheimer’s Disease patients can be characterized in three stages. In its comparatively mild early stage, people may get lost or have trouble handling money or daily tasks. Some personality and behavioral changes are also typical. Once people have trouble recognizing family and friends, Alzheimer’s Disease is classified as moderate; “damage occurs in areas of the brain that control language, reasoning, sensory processing, and conscious thought. People at this stage may have hallucinations, delusions, and paranoia and may behave impulsively.” [3]

By the time the disease has progressed to its most severe form, the brain has shrunken; people at this stage cannot communicate and are completely dependent on their caretakers. Most people with Alzheimer’s Disease become symptomatic in their senior years, though a small percentage have an early-onset form of the disease; early-onset Alzheimer’s Disease is usually due to genetic predisposition. [4] Current biomedical treatments may help memory, communication, and behavior, but they do not alter the underlying process of the disease. [5] These approaches focus on maintaining mental functioning, delaying symptoms, and include current drug therapies that regulate neurotransmitters, [6] but they do not prevent the progression in the long-term. [7]

Over 5 million people in the US suffer from Alzheimer’s Disease, which is an enormous societal cost. From a purely financial standpoint, The Alzheimer’s Association estimates that the USA costs in 2016 total $236 billion. This, however, is only one element of the great burden Alzheimer’s Disease places on patients and their families. Day-to-day care may put a physical strain on caretakers taking responsibility for all aspects of patients’ daily lives.

Above all else is the emotional affliction from experiencing the deterioration of a loved one. Like any terminal disease, friends and family bear the knowledge that it will, eventually, be fatal. Meanwhile, changes in personality and behavior may be alarming. In earlier stages, this may present as irritability or depression; eventually those with Alzheimer’s Disease will not recognize even those closest to them. In addition, patients may become agitated — physical or verbal outbursts are not uncommon — and they may experience delusions and hallucinations. [8] The profound costs of the disease make Alzheimer’s Disease research imperative; the ability to recuperate cognitive functioning would provide incredible relief to millions of Alzheimer’s Disease patients and their caretakers.

Memory loss is a defining characteristic of Alzheimer’s Disease. Much of the research in this field is focused on the hippocampus, part of the limbic system in the brain. The hippocampus is involved in both short and long-term memory. While previously thought to involve two separate processes, new evidence suggests that the neural mechanisms underlying short and long-term memories may be similar. [9] “Neuropsychological evidence suggests that the hippocampus is critical when associative information is involved (for review, see Jonides et al., 2008), in line with its proposed function as a relational binder in long-term memory (Cohen and Eichenbaum, 1993)... One possibility is that the hippocampus supports short-term memory for associative information through transient changes in synaptic efficacy, rather than active maintenance (Jonides et al., 2008).” [10] The post-mortem tests conducted on the mice in this study involved two aspects of hippocampal involvement: Aβ plaque accumulation and changes in BDNF.

The role of Aβ in Alzheimer’s Disease is perhaps best studied. Dr. Alois Alzheimer cared for a patient with the symptoms now known as Alzheimer’s Disease and discovered the Aβ plaque during an autopsy. [11] Further studies have concluded that the “pathological features of Alzheimer’s Disease include the accumulation of extracellular senile plaques predominantly composed of β-amyloid (Aβ) peptide, intracellular neurofibrillary tangles and neuronal loss, particularly in the hippocampus.” [12] Since an increase in Aβ is positively correlated with cognitive impairment, it can be reasoned that a decrease in Aβ may aid in recovery of cognitive function. The current study shows that electroacupuncture at DU20 decreases Aβ levels, and that the decrease is correlated with positive cognitive change.

Changes in the status of BDNF atre understood to be correlated with the progression of Alzheimer’s Disease; the researchers have further investigated its role. “Studies indicated that the precursor of BDNF (proBDNF), mature BDNF (mBDNF) and BDNF mRNA [messenger ribonucleic acid] expression levels were decreased in individuals with Alzheimer’s Disease, and the levels of BDNF were positively correlated with cognitive measures.” [13] BDNF is synthesized as proBDNF and is cleaved to form mBDNF. [14] It is believed that the processing thereof is key to the regulation of cellular function. These forms play different roles in the brain. “ProBDNF preferentially binds to the p75 neurotrophin receptor (p75NTR) leading to downstream signaling, via signaling pathways involved in apoptosis, and facilitating long-term depression in the hippocampus,” [15] thus suppressing proliferation of hippocampal neurons.

Apoptosis is programmed cell death. The life span of each cell is programmed into its DNA. Apoptosis is necessary; too little causes unchecked regeneration as in cancer cells and too much can cause atrophy. Whereas proBDNF was associated with increased atrophy, “cleaved mBDNF binds to the tropomyosin receptor kinase B (TrkB) receptor, promotes cell survival and facilitates certain forms of long-term potentiation.” [16] This indicates that the balance between proBDNF and mBDNF is crucial to the proper functioning of the brain. The researchers found that the overall level of BDNF was decreased in the Alzheimer’s Disease type mice, and also that the ratio between mBDNF and proBDNF was decreased, skewing the function away from long-term proliferation and toward hippocampal cell death. Additionally, BDNF exerts neuroprotective effects against Aβ, [17] which may speak to its unique importance in the pathogenesis of Alzheimer’s Disease.

To ensure that their findings were thorough, the researchers used four test groups. They had two control groups (one healthy and one Alzheimer’s Disease type) and two electroacupuncture test groups (one at DU20 and one a non-acupoint above the iliac and lateral to the spine). A healthy control group was included to compare normal levels of Aβ and BDNF and to gauge the degree of change. The non-acupoint control was included to ensure that the particular effect attributed to DU20 is not solely an effect of electroacupuncture in general.

The Alzheimer’s Disease type mice used were APP/PS1 double-transgenic mice, and those used in the control were their wild-type littermates. “APP/PS1 transgenic mice exhibit early onset and a high degree of Aβ deposition, followed by neuronal loss and cognitive impairment… [They] are considered to be reliable and effective models that are widely used in Alzheimer’s Disease research.” [18] After four weeks of electroacupuncture for thirty minutes daily, the mice were given the Morris water maze test to discern memory and spatial learning. They were placed in the maze each day over four days for exploration (to locate a platform), and on the fifth day their success was analyzed.

The DU20 Alzheimer’s Disease test group found the platform an average of slightly over three times in 90 seconds; the wild-type healthy control group found it on average slightly less than four times. Both the Alzheimer’s Disease control and non-acupoint groups found the platform once on average. Over the four days of exploration, the time it took the DU20 test group to find the platform was nearly midway between the wild-type and Alzheimer’s Disease type test groups, and the length of their path was likewise midway. While middling hardly seems like a positive response, the DU20 test path is a tidy spiral circling the maze as compared to the other Alzheimer’s Disease types that zigzag across the maze. The coherence of their path clearly demonstrates improvements in cognitive functioning.

Remarkably, the post-mortem findings of the DU20 electroacupuncture group show a decrease in Aβ and a relative normalization of the BDNF ratio, known factors of the disease. This clearly shows that electroacupuncture at DU20 can, at least partially, reverse the pathogenesis of Alzheimer’s Disease. Current therapies slow the progress of deterioration, but this discovery gives hope that it may be possible to reverse some of the damage done to the hippocampus. In human trials, it may be possible to alleviate the cognitive symptoms of Alzheimer’s Disease and benefit the structural integrity of the brain. This research elucidates electroacupuncture’s biochemical mechanisms of action at DU20 and how it affects cognitive function. This indicates that further investigation into the use of electroacupuncture for the treatment of Alzheimer’s Disease is warranted.



1 Lin, Ruhui, Jixiang Chen, Xiaojie Li, Jingjie Mao, Yunan Wu, Peiyuan Zhuo, Yinzheng Zhang, Weilin Liu, Jia Huang, Jing Tao, and Li-Dian Chen. "Electroacupuncture at the Baihui acupoint alleviates cognitive impairment and exerts neuroprotective effects by modulating the expression and processing of brain-derived neurotrophic factor in APP/PS1 transgenic mice." Molecular Medicine Reports, 2015. doi:10.3892/mmr.2015.4751. Pg 1611
2 pg2
3 pg 3.
4 Ibid, pg 3.
5 Ibid, pg 7.
6 Ibid, pg 6.
7 Ibid, pg 5.
8 Ibid, pg 3.
9 Wang, Zhiqun, Peipeng Liang, Zhilian Zhao, Ying Han, Haiqing Song, Jianyang Xu, Jie Lu, and Kuncheng Li. "Acupuncture Modulates Resting State Hippocampal Functional Connectivity in Alzheimer Disease." PLoS ONE 9, no. 3 (2014). doi:10.1371/journal.pone.0091160. Pg 3837.
10 Zhiqun Wang, Acupuncture Modulates Resting State Hippocampal Functional Connectivity. Pg 3838.
11 pgs 1-2.
12 Ruhui Lin et al, Electroacupuncture at the Baihui acupoint alleviates cognitive impairment, pg 1611.
13 Ibid, pg 1611.
14 Ibid, pg 1611.
15 Ibid, pg 1611-2.
16 Ibid, pg 1612.
17 Ibid, pg 1612.
18 Ibid, pg 1616.



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