Plasmalogens and Alzheimer Disease

Table of Contents

1. What Plasmalogens Are
2. Lower Plasmalogens in the Alzheimer Brain
3. Lower Plasmalogens in the Blood
4. The Proposed Mechanisms
5. The Scallop Plasmalogen Trial in Mild Alzheimer Disease
6. Other Supplement Trials in People
7. Food Sources Reported in Studies
8. What Is Not Known
9. Key Research Papers
10. Connections
11. Featured Videos

What Plasmalogens Are

Every cell is wrapped in a thin double layer of fat-like molecules called phospholipids. Plasmalogens are one family of phospholipids with an unusual joint. In most phospholipids, both fatty tails are attached by an ordinary chemical link called an ester bond. In a plasmalogen, the first tail is attached by a different link, a vinyl-ether bond, and the second tail is usually a polyunsaturated fatty acid such as docosahexaenoic acid (DHA) or arachidonic acid. Because of that ether link, chemists group them with the "ether phospholipids".

• How common they are. A 2012 review by Braverman and Moser states that plasmalogens make up as much as 20% of the total phospholipid mass in the human body. Their exact jobs have been hard to pin down and appear to differ from tissue to tissue.
• Where they are concentrated. A 2009 paper on newborns describes them as particularly abundant in the nervous system, the heart and the skeletal (striated) muscles. Reviews list roles in myelin, the fatty insulation around nerve fibres, in "lipid rafts" (small organised patches of the cell membrane), and in the cell's response to oxidation.
• Where they are made. The first steps of plasmalogen production happen inside peroxisomes, small compartments inside the cell that also break down very long fatty acids. Braverman and Moser describe a rare inherited malformation syndrome, rhizomelic chondrodysplasia punctata, caused by defects in these peroxisomal steps. Its features point to roles for plasmalogens in the development of bone, brain, eye lens, lung, kidney and heart.
• Two main types. Most measurements in Alzheimer research concern ethanolamine plasmalogens, the form that dominates in the brain. A smaller group of studies measures choline plasmalogens.

Because the body makes its own plasmalogens, they are not a vitamin. The questions on this page are whether levels fall in Alzheimer disease, whether that fall matters, and whether taking them by mouth changes anything.

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Lower Plasmalogens in the Alzheimer Brain

The first evidence came from brain tissue examined after death. Several independent groups, using different methods and different brain banks, reported the same direction of change.

Specific to the regions Alzheimer disease damages (1995)

Ginsberg and colleagues reported a significant and selective shortage of ethanolamine plasmalogen, compared with its ordinary ester-linked relative, in brains from people who had Alzheimer disease. The shortage was greater in the mid-temporal cortex, a region the disease damages, than in the cerebellum, a region it largely spares. It was not seen in the main damaged region of Huntington disease (the caudate nucleus) or of Parkinson disease (the substantia nigra). The authors linked it to a tendency of Alzheimer brain membranes to become unstable.

Already present at the very mild stage (2001)

Han, Holtzman and McKeel measured plasmalogens in grey and white matter from people across the Clinical Dementia Rating scale, which runs from 0.5 (very mild dementia) to 3 (severe dementia). Their abstract reports:

• a decrease of up to 40 mol% of total plasmalogen in white matter at the very earliest stage studied (rating 0.5);
• in grey matter, a shortage that grew with dementia severity, from about 10 mol% at rating 0.5 to about 30 mol% at rating 3;
• no change in plasmalogen content in the grey matter of the cerebellum at any stage, although cerebellar white matter did change.

In two strains of mice bred to develop Alzheimer-like amyloid deposits, the same team found a shortage of up to 10 mol% in the cerebral cortex at 18 months of age, and none in the cerebellum.

A large drop in choline plasmalogen (2011)

Igarashi and colleagues at the United States National Institute on Aging measured absolute lipid amounts in the prefrontal cortex of 10 people with Alzheimer disease and 9 without. Total brain lipid, phospholipid, cholesterol and triglyceride did not differ between the groups. Choline plasmalogen, however, was 73% lower in the Alzheimer group, while the other measured phospholipids did not differ. The authors read the pattern as a sign of extensive remodelling of brain membranes. The sample was small.

Linked to tangles and to peroxisome changes (2011)

Kou and colleagues studied brains from the Vienna-Transdanube Aging study, grouped by Braak stage, the standard scale of how far tau tangles have spread. In the most severely affected brains (stages V–VI), plasmalogens were lower and very long-chain fatty acids, which peroxisomes normally break down, had built up. Both changes pointed toward failing peroxisomes. The fall in plasmalogens was more closely tied to the amount of neurofibrillary tangles than to the amount of amyloid plaques.

One plasmalogen tracked memory before death (2022)

A 2022 analysis of the inferior temporal cortex of 100 elderly people from the Rush Memory and Aging Project (average age 88.5 years; 38 without cognitive impairment, 24 with mild cognitive impairment and 38 with Alzheimer dementia) measured individual plasmalogen species alongside tangles, amyloid and a lipid-raft protein. After statistical adjustment, the DHA-carrying ethanolamine plasmalogen called PL 18:0/22:6 (β = 0.506), tangles and the raft protein were independently associated with cognition near the time of death. The link between high DHA-plasmalogen levels and better cognition held regardless of plaque and tangle load. The paper's authors worked for a company that develops plasmalogen precursors.

These are snapshots of brains at death. They show that levels were lower; they cannot show whether the shortage came first or followed from the disease.

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Lower Plasmalogens in the Blood

Brain tissue can only be studied after death, so researchers asked whether a similar change shows up in the blood.

• Five population collections (2007). Goodenowe and colleagues measured ethanolamine plasmalogens in serum from five independent collections that together included more than 400 people with dementia and more than 350 without. Serum levels were significantly lower in people with clinically or pathologically diagnosed dementia of the Alzheimer type at all stages of dementia, and the size of the drop tracked the severity of dementia. A linear regression model in the paper predicted that serum levels fall years before symptoms appear; that is a model estimate, not a measurement in people followed over time. The authors argued in the title that the shortage is "a logical causative factor", which is their hypothesis.
• A one-year pilot (2010). Wood and colleagues measured serum DHA plasmalogen in 40 people with Alzheimer disease and retested their thinking with the Alzheimer Disease Assessment Scale–Cognitive one year later. Scores worsened significantly in those whose plasmalogen level at the start was at or below 75% of the level in age-matched controls, and did not change in those above 75%. The authors called it a pilot needing confirmation in a larger group.
• Japanese trial participants (2020). In a book chapter describing their trial work, Fujino, Hossain and Mawatari report that baseline plasma and red-cell ethanolamine plasmalogens were significantly lower in people with mild cognitive impairment, Alzheimer disease and Parkinson disease than in healthy older people, with the reduction increasing in the order mild cognitive impairment, mild, moderate and severe Alzheimer disease, then Parkinson disease. They propose blood plasmalogens as a marker of severity.

A 2026 narrative review in the Journal of Agricultural and Food Chemistry summarises the human data the same way: plasmalogen levels decline with age, and the decline is steeper in Alzheimer disease. A 2025 review from the United States National Institutes of Health notes that low plasmalogen levels are also reported in heart, kidney and liver disease, in cancer and in rare peroxisomal disorders, so a low level is not specific to Alzheimer disease.

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The Proposed Mechanisms

None of the explanations below has been proven in people. Each is a proposal drawn from cell, animal or post-mortem work, and the sentences say which.

Failing peroxisomes (proposed)

Because plasmalogen production starts in peroxisomes, a shortage could reflect peroxisomes that work poorly. The Vienna post-mortem study found two signs of that together in severely affected brains: fewer plasmalogens and a build-up of very long-chain fatty acids. It also saw, under the microscope, a loss of peroxisomes from nerve-cell branches that carried abnormal tau, and suggested that disturbed transport inside the nerve cell moves peroxisomes to the wrong places. The 2007 serum paper adds that production runs through a single peroxisomal pathway that declines with age.

Membrane structure and synapses (proposed)

Ginsberg and colleagues linked the shortage to unstable membranes in the Alzheimer brain, and Han and colleagues suggested that it may contribute to synapse loss and poor synaptic function. Both are inferences from tissue measurements.

Effects on amyloid production (in laboratory tests)

Rothhaar and colleagues tested plasmalogen species in laboratory preparations of cell membranes and in post-mortem Alzheimer brain tissue. Every species tested lowered the activity of gamma-secretase, one of the enzymes that cuts the amyloid precursor protein into amyloid-beta. The authors proposed a vicious cycle: amyloid-beta lowers plasmalogens, and lower plasmalogens let gamma-secretase make more amyloid-beta. This was not tested in living people.

Inflammation in brain support cells (in mice and cells)

Hossain and colleagues found that inflammatory signals lowered plasmalogen levels in mouse glial cells by switching down the enzyme that starts plasmalogen production, through the NF-kappa-B pathway. In mice, ageing, chronic restraint stress and injected bacterial toxin all lowered brain plasmalogens. Lowering plasmalogens in the mouse cortex in turn made microglia, the brain's immune cells, more active. The same enzyme change was seen in human cell lines, in a mouse model of Alzheimer disease and in post-mortem human Alzheimer brain tissue. Hossain is a co-author of the 2020 chapter on the scallop plasmalogen trials described below.

An antioxidant role (proposed and disputed)

The vinyl-ether bond reacts readily with oxidising molecules. One long-standing idea is that plasmalogens act as sacrificial antioxidants that take the damage in place of other membrane fats. Lessig and Fuchs, in a 2009 review, call this role controversial: the products of plasmalogen oxidation themselves build up in atherosclerosis, heart attack, ageing and Alzheimer disease. Reviews from 2019 and 2025 still list antioxidant and redox roles among plasmalogen functions.

Cause or consequence

The proposals point both ways. Some treat the shortage as an early driver; the inflammation work and the amyloid work both describe the disease process itself lowering plasmalogens. The evidence available does not settle which comes first.

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The Scallop Plasmalogen Trial in Mild Alzheimer Disease

The main trial in people with memory disease was published by Fujino and colleagues in EBioMedicine in 2017. It is the trial most often cited for plasmalogen supplements, so its design and results are set out in full.

• Design. Multicentre, randomised, double-blind, placebo-controlled, 24 weeks, in Japan. Registered as UMIN000014945.
• Who took part. 328 people aged 60 to 85 with Mini-Mental State Examination (Japanese version) scores of 20 to 27 and little or no depression. Scores of 20–23 were classed as mild Alzheimer disease; scores of 24–27 as mild cognitive impairment.
• What they took. The trial gave 1 mg a day of plasmalogens purified from scallop, or a placebo.
• Who finished. 276 of 328 (140 in the plasmalogen group, 136 on placebo).
• Primary outcome. Change in the Mini-Mental State Examination score.
• Secondary outcomes. The Wechsler Memory Scale–Revised, a depression scale, and plasmalogen levels in red cells and plasma.

Results

• Primary outcome not met. In the intention-to-treat analysis of everyone randomised (mild Alzheimer disease and mild cognitive impairment together), there was no significant difference between plasmalogen and placebo in the primary outcome or in any secondary outcome.
• Safety. No severe adverse events in either group.
• Mild Alzheimer disease group. Memory scores (Wechsler Memory Scale–Revised) improved significantly within the plasmalogen group, but the difference between plasmalogen and placebo was not statistically significant (P = 0.067).
• Subgroups. Within the mild Alzheimer disease group, further subgroup analyses found significant between-group differences in memory scores in women (P = 0.017) and in people younger than 77 (P = 0.029). These subgroup analyses are not the trial's main test; the abstract does not describe them as planned in advance, and results found by splitting a trial into smaller groups need a new trial to confirm them.
• Blood levels. Among people with mild Alzheimer disease, plasma ethanolamine plasmalogen fell significantly more in the placebo group than in the plasmalogen group.

The authors concluded that scallop plasmalogens "may improve cognitive functions of mild AD". The trial was funded by the Japanese Plasmalogen Society.

The open-label extensions

The 2020 book chapter by Fujino, Hossain and Mawatari describes, alongside the randomised trial, three studies with no placebo group: 12 weeks in moderate Alzheimer disease (57 people), 12 weeks in severe Alzheimer disease (18 people) and 24 weeks in Parkinson disease (10 people). The authors report significant improvement in cognitive function and other symptoms with rising blood plasmalogen levels, and no adverse events. Because everyone knew they were receiving the supplement and there was no comparison group, these studies cannot separate an effect of plasmalogens from the placebo effect, practice on repeated tests, or chance.

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Other Supplement Trials in People

The remaining randomised trials found in PubMed were run in people without a dementia diagnosis. They say nothing directly about treating Alzheimer disease, but they are the rest of the human evidence.

• Ascidian plasmalogen in adults with mild forgetfulness (2020). Watanabe and colleagues randomised 49 healthy Japanese adults (average age about 46) to a food containing 1 mg of plasmalogen from sea squirt (ascidian) or a placebo food for 12 weeks. On the Cognitrax computer test battery, composite memory rose more in the plasmalogen group than in the placebo group (by 3.0 ± 16.3 points at 8 weeks and 6.7 ± 17.5 points at 12 weeks).
• Scallop plasmalogen in healthy middle-aged and older adults (2026). Fukuchi and colleagues randomised 68 cognitively healthy Japanese adults aged 40 or over with below-average verbal memory to 1 mg a day of scallop plasmalogens or placebo for 12 weeks; 66 were analysed. The primary outcome, the standardised verbal memory score, was higher in the plasmalogen group (difference 10.1 points; 95% confidence interval 0.4 to 19.9; p = 0.042). Blood levels of brain-derived neurotrophic factor rose in both groups with no difference between them. No adverse events were reported. Two authors were employed by, or held shares in, a company, according to the paper's conflict-of-interest statement, and the authors call for further studies to confirm the findings.
• Scallop plasmalogen in college athletes (2022). Fujino and colleagues randomised 40 male university athletes to 2 mg a day or placebo for 4 weeks. The primary outcome, the Total Mood Disturbance score, did not reach statistical significance (p = 0.07). Some secondary scores, anger-hostility (p = 0.003) and fatigue-inertia (p = 0.005), and a timed concentration test favoured the plasmalogen group. This was a mood trial in young men, not a memory-disease trial.
• A combined product in older adults (2024). Yamada and colleagues gave healthy older Japanese people a supplement combining ascidian plasmalogen with elastin, or placebo, for 16 weeks (123 analysed per protocol). Selected categories of the Rivermead Behavioural Memory Test, such as remembering a first name and face recognition, scored higher in the supplement group, with further differences in subgroups of people 75 or older and of women. Because two ingredients were given together, the trial cannot show what plasmalogen alone did.

One further small study, an uncontrolled trial of a synthetic DHA plasmalogen precursor in 22 cognitively impaired people published in 2022, carried an expression of concern in January 2026 and was retracted by its journal in August 2026. It is not used as evidence on this page.

A PubMed search in November 2026 found no meta-analysis or systematic review that pools plasmalogen supplement trials for dementia or cognition. Reviews such as Paul, Lancaster and Meikle (2019) describe other ways researchers have tried to raise plasmalogen levels, including inositol and naturally occurring precursors called alkylglycerols, mostly in animal and early clinical work.

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Food Sources Reported in Studies

Plasmalogens are made by animals, so the foods that contain them are animal foods. Laboratory surveys of food give these findings:

• A wide range of amounts. Yamashita and colleagues (2016) measured ethanolamine plasmalogen in a range of foods and found from 5 to 549 µmol per 100 g of wet weight. Marine invertebrates had the most: blue mussel and ascidian (sea squirt) were each above 200 µmol per 100 g. In seafood, the plasmalogens mainly carried the omega-3 fats eicosapentaenoic acid (EPA) and DHA; in foods from land animals they mainly carried arachidonic acid. In cells grown in the laboratory, a plasmalogen-rich fraction from ascidian protected nerve-like cells from dying under stress better than one from cow brain.
• Meat, poultry and seafood. Wu and colleagues (2021) measured plasmalogens in 14 kinds of livestock, poultry and seafood. Squid and octopus plasmalogens were especially rich in EPA, which made up 98.4% and 94.5% of their plasmalogen fatty acids respectively.
• Cooking reduces them. In beef, Wu and colleagues (2020) found that roasting and frying caused significant losses of plasmalogen that grew with cooking temperature and time, with extra loss at the fried surface compared with the core. A batter coating reduced the loss during frying.
• The trial material. The trials above used plasmalogens purified from scallop or from ascidian, at 1–2 mg a day.

No study found here measured whether eating shellfish or meat changes brain plasmalogen levels or the risk of Alzheimer disease in people. For the wider evidence on seafood fats and the brain, see the Omega-3 Fatty Acids for Brain and Cognition page, and for organ meats see Organ Meats for Brain and DHA.

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What Is Not Known

• Cause or effect. Lower plasmalogens in the brain and blood are well documented, but whether the shortage helps cause Alzheimer disease or is a result of it is unresolved. The cell and mouse work supports both directions.
• Whether the supplement works in Alzheimer disease. The one randomised trial in people with mild Alzheimer disease or mild cognitive impairment did not meet its primary outcome. The positive signals came from a subgroup that fell short of significance and from smaller subgroups within it. No independent trial has repeated it.
• Moderate and severe disease. The only data come from open-label studies with no placebo group.
• Size and setting. All the randomised trials were small, short (4 to 24 weeks) and run in Japan. The 2017 trial was funded by the Japanese Plasmalogen Society, and the 2026 trial had company-employed authors. No randomised trial has been reported from outside Japan.
• Whether swallowed plasmalogens reach the brain. The 2017 trial measured plasma and red-cell levels, not brain levels. How much of an oral dose reaches human brain tissue has not been measured.
• Long-term safety. The trials reported no serious adverse events over periods of up to six months. The 2026 trial authors note that long-term safety still needs study.
• Hard outcomes. No trial has measured progression to dementia, need for care, or brain changes on scans.
• Diet. No human study links dietary plasmalogen intake to Alzheimer risk.

Questions about any supplement for memory problems are for a clinician who knows the person's medicines and history.

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Key Research Papers

1. Ginsberg L, Rafique S, Xuereb JH, Rapoport SI, Gershfeld NL. Disease and anatomic specificity of ethanolamine plasmalogen deficiency in Alzheimer's disease brain. Brain Res. 1995;698(1-2):223-6. PubMed PMID: 8581486
2. Han X, Holtzman DM, McKeel DW Jr. Plasmalogen deficiency in early Alzheimer's disease subjects and in animal models: molecular characterization using electrospray ionization mass spectrometry. J Neurochem. 2001;77(4):1168-80. PubMed PMID: 11359882
3. Goodenowe DB, Cook LL, Liu J, Lu Y, Jayasinghe DA, Ahiahonu PW, et al. Peripheral ethanolamine plasmalogen deficiency: a logical causative factor in Alzheimer's disease and dementia. J Lipid Res. 2007;48(11):2485-98. PubMed PMID: 17664527
4. Wood PL, Mankidy R, Ritchie S, Heath D, Wood JA, Flax J, et al. Circulating plasmalogen levels and Alzheimer Disease Assessment Scale-Cognitive scores in Alzheimer patients. J Psychiatry Neurosci. 2010;35(1):59-62. PubMed PMID: 20040248
5. Igarashi M, Ma K, Gao F, Kim HW, Rapoport SI, Rao JS. Disturbed choline plasmalogen and phospholipid fatty acid concentrations in Alzheimer's disease prefrontal cortex. J Alzheimers Dis. 2011;24(3):507-17. PubMed PMID: 21297269
6. Kou J, Kovacs GG, Höftberger R, Kulik W, Brodde A, Forss-Petter S, et al. Peroxisomal alterations in Alzheimer's disease. Acta Neuropathol. 2011;122(3):271-83. PubMed PMID: 21594711
7. Goodenowe DB, Senanayake V. Brain ethanolamine phospholipids, neuropathology and cognition: A comparative post-mortem analysis of structurally specific plasmalogen and phosphatidyl species. Front Cell Dev Biol. 2022;10:866156. PubMed PMID: 36092723
8. Braverman NE, Moser AB. Functions of plasmalogen lipids in health and disease. Biochim Biophys Acta. 2012;1822(9):1442-52. PubMed PMID: 22627108
9. Labadaridis I, Moraitou M, Theodoraki M, Triantafyllidis G, Sarafidou J, Michelakakis H. Plasmalogen levels in full-term neonates. Acta Paediatr. 2009;98(4):640-2. PubMed PMID: 19290965
10. Lessig J, Fuchs B. Plasmalogens in biological systems: their role in oxidative processes in biological membranes, their contribution to pathological processes and aging and plasmalogen analysis. Curr Med Chem. 2009;16(16):2021-41. PubMed PMID: 19519379
11. Rothhaar TL, Grösgen S, Haupenthal VJ, Burg VK, Hundsdörfer B, Mett J, et al. Plasmalogens inhibit APP processing by directly affecting γ-secretase activity in Alzheimer's disease. ScientificWorldJournal. 2012;2012:141240. PubMed PMID: 22547976
12. Hossain MS, Abe Y, Ali F, Youssef M, Honsho M, Fujiki Y, et al. Reduction of Ether-Type Glycerophospholipids, Plasmalogens, by NF-κB Signal Leading to Microglial Activation. J Neurosci. 2017;37(15):4074-4092. PubMed PMID: 28292831
13. Paul S, Lancaster GI, Meikle PJ. Plasmalogens: A potential therapeutic target for neurodegenerative and cardiometabolic disease. Prog Lipid Res. 2019;74:186-195. PubMed PMID: 30974122
14. Curran CS, Remaley AT, Torabi-Parizi P. Plasmalogens as biomarkers and therapeutic targets. J Lipid Res. 2025;66(12):100925. PubMed PMID: 41130295
15. Fujino T, Yamada T, Asada T, Tsuboi Y, Wakana C, Mawatari S, et al. Efficacy and Blood Plasmalogen Changes by Oral Administration of Plasmalogen in Patients with Mild Alzheimer's Disease and Mild Cognitive Impairment: A Multicenter, Randomized, Double-blind, Placebo-controlled Trial. EBioMedicine. 2017;17:199-205. PubMed PMID: 28259590
16. Fujino T, Hossain MS, Mawatari S. Therapeutic Efficacy of Plasmalogens for Alzheimer's Disease, Mild Cognitive Impairment, and Parkinson's Disease in Conjunction with a New Hypothesis for the Etiology of Alzheimer's Disease. Adv Exp Med Biol. 2020;1299:195-212. PubMed PMID: 33417216
17. Watanabe H, Okawara M, Matahira Y, Mano T, Wada T, Suzuki N, et al. The Impact of Ascidian (Halocynthia roretzi)-derived Plasmalogen on Cognitive Function in Healthy Humans: A Randomized, Double-blind, Placebo-controlled Trial. J Oleo Sci. 2020;69(12):1597-1607. PubMed PMID: 33177278
18. Fujino M, Fukuda J, Isogai H, Ogaki T, Mawatari S, Takaki A, et al. Orally Administered Plasmalogens Alleviate Negative Mood States and Enhance Mental Concentration: A Randomized, Double-Blind, Placebo-Controlled Trial. Front Cell Dev Biol. 2022;10:894734. PubMed PMID: 35721497
19. Yamada S, Shirai M, Katsumata M, Kurono M, Matahira Y, Ono K, et al. Beneficial Effects of a Formulated Supplement of Ascidiacea (Halocynthia-roretzi)-derived Plasmalogen and Tuna-derived Elastin on Memory Function in Elderly Japanese Subjects; A Randomized, Double-blind, Placebo-controlled Study. J Oleo Sci. 2024;73(10):1319-1328. PubMed PMID: 39313395
20. Fukuchi M, Tanaka M, Nagata M, Takara T, Sasuga Y. Orally administered scallop-derived plasmalogens improve cognitive function in healthy middle-aged and older adults: a randomized, double-blind, placebo-controlled trial. Front Nutr. 2026;13:1906996. PubMed PMID: 42656342
21. Yamashita S, Kanno S, Honjo A, Otoki Y, Nakagawa K, Kinoshita M, et al. Analysis of Plasmalogen Species in Foodstuffs. Lipids. 2016;51(2):199-210. PubMed PMID: 26732602
22. Wu Y, Chen Z, Chiba H, Hui SP. Plasmalogen fingerprint alteration and content reduction in beef during boiling, roasting, and frying. Food Chem. 2020;322:126764. PubMed PMID: 32325364
23. Wu Y, Chen Z, Jia J, Chiba H, Hui SP. Quantitative and Comparative Investigation of Plasmalogen Species in Daily Foodstuffs. Foods. 2021;10(1):124. PubMed PMID: 33435634
24. Zhang Y, Chen J, Jiang J, Yang N, Guo S, Gao F, et al. Plasmalogens in Alzheimer's Disease: A Narrative Review of Dietary Sources, Metabolism, and Neuroprotective Mechanisms. J Agric Food Chem. 2026;74(25):19375-19392. PubMed PMID: 42310520

PubMed Topic Searches

1. PubMed: plasmalogens in the Alzheimer brain
2. PubMed: blood plasmalogens and dementia
3. PubMed: plasmalogen supplement trials and cognition
4. PubMed: peroxisomes, plasmalogens and Alzheimer disease
5. PubMed: plasmalogens in foods

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Connections

• Alzheimer's Disease — the main page on the disease
• Alzheimer's Disease: History and Discovery — how the disease came to be understood
• Dementia — the wider group of conditions
• Omega-3 Fatty Acids for Brain and Cognition — the DHA that plasmalogens often carry
• Organ Meats for Brain and DHA — animal foods and brain fats
• Phosphorus for Cell Membranes — the phospholipid family plasmalogens belong to
• Serine for Phosphatidylserine and the Aging Brain — another membrane phospholipid studied for memory
• Choline for Cognition — the head group of choline plasmalogens

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