Integrating repetitive transcranial magnetic stimulation and Mediterranean diet for cognitive and anxiety improvement in early Alzheimer's disease: A case report and literature review

Abstract

A 52-year-old male with early-stage Alzheimer's disease and long-standing anxiety received 30 repetitive transcranial magnetic stimulation sessions over 8 months and 20-month Mediterranean diet intervention. Neuropsychological assessments [Montreal Cognitive Assessment (MoCA), Mini-Mental State Examination (MMSE), Clinical Dementia Rating, Hamilton Anxiety Rating Scale (HAMA), Hamilton Depression Rating Scale (HAMD), Pittsburgh Sleep Quality Index) and resting-state electroencephalogram (rsEEG) were conducted at baseline, during treatment, and at 6-month follow-up. After treatment, MoCA and MMSE scores improved by 6 and 5 points; HAMA and HAMD scores declined by 7 and 3 points. rsEEG showed progressive increases in individual alpha peak frequency (8.69 to 10.22 Hz), enhancement of alpha power, and reduction in theta power. Cerebrospinal fluid amyloid-β₄₂ levels also normalized. The patient reported marked mental well-being.

Keywords

Alzheimer's disease anxiety electroencephalogram individual alpha peak frequency Mediterranean diet repetitive transcranial magnetic stimulation

Introduction

Alzheimer's disease (AD), a leading cause of dementia, is frequently accompanied by neuropsychiatric symptoms that significantly affect disease progression and patient quality of life.¹ Anxiety disorders are notably prevalent, with studies indicating that approximately 40% of individuals with AD experience anxiety symptoms.² Traditional pharmacological treatments for AD with comorbid anxiety typically involve selective serotonin reuptake inhibitors or benzodiazepines. However, long-term use of these drugs may exacerbate cognitive decline and potentially accelerate the progression of AD.^3,4

Repetitive transcranial magnetic stimulation (rTMS) is a safe and non-invasive treatment using rapidly changing magnetic fields to modulate the electrical activity of the brain.⁵ Low-frequency (≤1 Hz) rTMS exhibits inhibitory effects, whereas high-frequency (≥5 Hz) shows excitatory effects on brain activity.^6,7 A large number of clinical studies have suggested high-frequency rTMS as a promising treatment for mild cognitive impairment (MCI) and AD dementia,^8,9 while low-frequency for insomnia and anxiety disorders.^10,11

The Mediterranean diet (MedDiet) is widely recognized as a healthful dietary pattern for prevention of cardiovascular, metabolic, and neurodegenerative diseases.¹² It is characterized by a high intake of plant-based foods and olive oil, along with moderate consumption of fish and poultry, limited red meat, and moderate dairy intake.^12,13 This diet has been associated with numerous health benefits and is the primary dietary recommendation for managing MCI in clinical guidelines.¹⁴ Adherence to the MedDiet has been shown to improve cognitive function and alleviate symptoms of anxiety.^15,16 However, the combination of rTMS with the MedDiet has rarely been explored in clinical settings.

Here, we report a patient with prodromal AD and a 30-year history of severe anxiety disorder who experienced significant cognitive and anxiety symptom relief following treatment with rTMS combined with the MedDiet, providing a novel therapeutic strategy for AD with comorbid anxiety.

Case presentation

We report a 52-year-old male presented with a gradual memory impairment over several months, which affected his work and daily life. He had difficulty in recalling events from the previous day, including details of his breakfast. He also had a 30-year history of anxiety, for which he was on a combination of anxiolytic medications, including venlafaxine (600 mg/day), diazepam (7.5 mg/day), flupentixol (31.5 mg/day), aripiprazole (10 mg/day), and trihexyphenidyl (2 mg/day). His family has a history of AD in his mother and grandfather. Cognitive assessment revealed a Montreal Cognitive Assessment (MoCA) score of 22, a Mini-Mental State Examination (MMSE) score of 25, and a Global Clinical Dementia Rating (CDR) score of 0.5, indicating MCI. His Hamilton Anxiety Rating Scale (HAMA) and Hamilton Depression Rating Scale (HAMD) scores were 10 and 9, respectively. In addition, his sleep quality was tested by Pittsburgh Sleep Quality Index (PSQI), the score was 7, indicating mild sleep disturbance. Resting-state electroencephalogram (rsEEG) showed an individual alpha peak frequency (IAF) of 8.69 Hz, with abnormal relative power in alpha (0.22), beta (0.30), theta (0.31) bands and elevated theta/alpha (1.90) and theta/beta (4.80) ratios. Cerebrospinal fluid (CSF) biomarkers revealed a decreased in amyloid-β (Aβ)₄₂ (400 pg/mL, normal reference ≥ 650 pg/mL), while other AD markers were within normal limits. Genetic testing showed APOE ε4/ε4 genotype. MRI findings and his antibodies related to paraneoplastic syndrome, N-methyl-D-aspartate receptors (NMDARs), and leucine-rich glioma-inactivated 1 (LGI1) related to autoimmune encephalitis were normal. Other routine and metabolic laboratory tests, including those surveying poisoning, immunization, and infection, showed no abnormalities. Based on the National Institute on Aging-Alzheimer's Association 2011¹⁷ and Diagnostic and Statistical Manual-5 criteria, the patient was diagnosed with MCI due to AD, with comorbid anxiety disorder.

Prior to treatment, the patient exhibited irregular dietary habits, primarily following a traditional Chinese diet characterized by rice and wheat flour as staple foods, limited intake of vegetables and fruits, and a relatively high consumption of red meat. In response, we recommended the adoption of a MedDiet in conjunction with rTMS therapy.

The patient received three courses of rTMS, totaling 30 sessions over the first 8 months, which was applied by a figure-of-eight magnetic coil (Coil B658, external wing diameter 90 mm) connected to a MagPro 100 magnetic stimulator (MagVenture, Farum, Denmark). Resting motor threshold was defined as the minimum stimulus intensity producing a motor-evoked potential exceeding 50 μV in a minimum of five out of ten trials in the relaxed left abductor pollicis brevis.¹⁸ The first course, conducted during the first month, comprised five sessions over one week. It targeted the left and right dorsolateral prefrontal cortex (DLPFC) with 10 Hz and 1 Hz stimulation, respectively, delivering 1360 pulses per target per session. The second course included 20 sessions over months 2 to 4, targeting the left DLPFC and the precuneus (PCu), both stimulated with 10 Hz and 1360 pulses per target per session, administered twice weekly. The third and final course, initiated during months 7 to 8, consisted of 10 weekly sessions targeting the right DLPFC with 1 Hz stimulation.

In parallel, the patient consistently adhered to the MedDiet for 20 months, following a protocol adapted from the PREDIMED study,¹⁹ without caloric restriction. Dietary recommendations summarized in Figure 1, mainly included: consumption of ≥4 tablespoons/day of extra virgin olive oil; ≥2 servings/day of fresh vegetables; ≥3 servings/day of fresh fruit; ≥3 servings/week of tree nuts and peanuts; ≥3 servings/week of fish and seafood, particularly oily fish; ≥3 servings/week of legumes; ≥2 servings/day of sofrito (a traditional sauce made with tomato, garlic, onion, or leek, and simmered in olive oil); and preferential intake of white meat over red meat. Concurrently, anxiolytic medications were gradually tapered under the supervision of the attending physician and discontinued after 17 months. A comprehensive summary of the multimodal treatment plan is presented in Figure 1.

Figure 1.

Timeline of the treatment approach. This timeline illustrates the patient's clinical course, including three courses of rTMS (totaling 30 sessions over 8 months), sustained adherence to the MedDiet for 20 months, and discontinuation of psychiatric medications at month 17. It also highlights the assessment time points at months 7 and 12 during treatment, as well as a 6-month post-treatment follow-up (month 26). Blue shading indicates periods during which the patient received active interventions. # for the main components of the MedDiet.

Neuropsychological assessments were conducted at baseline, during the intervention (months 7 and 12), and at a 6-month post-treatment follow-up (month 26). All evaluations were performed by the same experienced neurologist at the Department of Neurology, Shenzhen People's Hospital to ensure consistency. After 12 months of combination therapy, the patient showed significant improvements in cognitive and emotional assessments compared to baseline, with MoCA and MMSE scores increasing by 5 and 4 points, respectively; the CDR score decreased from 0.5 to 0; and both HAMA and HAMD declined by 7 points. These improvements were maintained at the 6-month follow-up. However, the PSQI score rose from 7 to 12 after 12 months of treatment, but subsequently decreased back to 7 at follow-up. Detailed results are presented in Table 1.

Table 1.

Dynamic monitoring of treatment efficacy by cognitive scales and rsEEG.

	Results
Test items	Baseline	Month 7	Month 12	Month 26	Reference range (age and education-matched)
Neurological function assessment
MoCA	22	28	27	28	26–30
MMSE	25	29	29	30	27–30
CDR	0.5	0	0	0	0
HAMA	10	6	3	3	<7
HAMD	9	7	2	6	<7
PSQI	7	9	12	7	<7
rsEEG
Occipital IAF (Hz)	8.69	9.81	9.94	10.22	10.00
alpha relative power	0.22	0.33	0.26	0.44	N/A
theta relative power	0.31	0.09	0.14	0.15	N/A
beta relative power	0.30	0.41	0.42	0.25	N/A
delta relative power	0.11	0.10	0.14	0.12	N/A
theta / alpha ratio	1.90	0.30	0.60	0.40	N/A
theta / beta ratio	4.80	0.90	1.40	2.40	N/A

Results of cognitive, emotional, and rsEEG assessments at baseline, during treatment (months 7 and 12), and at 6-month follow-up (month 26). MoCA: Montreal Cognitive Assessment; MMSE: Mini-Mental State Examination; CDR: Clinical Dementia Rating; HAMA: Hamilton Anxiety Rating Scale; HAMD: Hamilton Depression Rating Scale; PSQI: Pittsburgh Sleep Quality Index; rsEEG: resting-state electroencephalography; IAF: individual alpha peak frequency.

rsEEG data with the eyes closed were acquired on the same day as the neuropsychological assessments using a 64-channel BrainAmp DC amplifier system (Brain Products, GmbH, Munich, Germany). The detailed steps were outlined in the paper of Yi et al.²⁰ The cleaned EEG data were then filtered into four canonical frequency bands: delta (1–4 Hz), theta (4–8 Hz), alpha (8–13 Hz), beta (13–30 Hz). The power spectral density estimates were obtained using the Welch method over 10 s epochs with 50% overlap, and subsequently averaged across epochs. Relative spectral power estimation in each frequency band was achieved by normalizing the source power to the broadband power at each channel location. The IAF peak was defined as the frequency point exhibiting the maximum power density within the range of 8 to 13 Hz, with an average taken over electrodes O1 and O2 according to the 10–20 EEG system. We found IAF in the occipital region increased from 8.69 Hz at baseline to 9.81 Hz (month 7), 9.94 Hz (month 12), and 10.22 Hz (month 26) (Figure 2A, B). At follow-up, the alpha relative power increased from 0.22 to 0.44, whereas the theta relative power decreased from 0.31 to 0.15, the theta/alpha ratio decreased from 1.90 to 0.40, and the theta/beta ratio decreased from 4.80 to 2.40 (Table 1). Furthermore, the alpha power distribution became more symmetrical, predominantly localized to the occipital region (Figure 2C).

Figure 2.

rsEEG features during all visits. (A) The change in IAF from baseline to the subsequent three visits progressively increased from approximately 8 Hz to 10 Hz; (B) PSD from all rsEEG channels at baseline and three following visits; (C) Topographical maps of relative power distribution of the theta, alpha, and beta bands under the eyes-closed condition. Over time, the relative power of the theta band decreased, while the power of the alpha band increased. Additionally, alpha power distribution became increasingly symmetrical, predominantly located in the occipital region. Red and blue indicate the relative power values, with blue representing lower values and red indicating higher values.

The neuropathological biomarkers of AD were measured by CSF at 6-month follow up. Lumbar puncture was carried out at the in-patient department according to standard procedures,²¹ and CSF analysis was performed using an ELISA assay (Euroimmun, Lübeck, Germany) according to the manufacturer's recommendations. The results demonstrated an elevated Aβ₄₂ level from 400 pg/mL to 750 pg/mL, whereas Aβ₄₂/Aβ₄₀ and p-tau 181 level remained within the normal range (Table 2).

Table 2.

AD-related neuroimaging findings and pathological test results.

	Results
Test items	Baseline	Month 26	Reference range (age and education-matched)
CSF tests
Aβ₄₂ (pg/mL)	400	750	≥ 650
Aβ₄₀ (pg/mL)	2700	6200	N/A
Aβ₄₂/Aβ₄₀ ratio	0.15	0.12	> 0.10
p-tau 181 (pg/mL)	19	45	≤ 61
T-tau (pg/mL)	220	370	< 290
Neuroimaging
Brain MRI	Normal	Normal	Normal
¹⁸F-AV45-PET	N/A	Negative	Negative
¹⁸F-AV1451-PET	N/A	Negative	Negative
Brain MRA	Negative	Negative	Negative
Gene sequencing
APOE	ε4/ε4	N/A	N/A

Results of the patient's AD-related assessments at baseline and at month 26. CSF: cerebrospinal fluid; MRI: magnetic resonance imaging; PET: positron emission tomography; ¹⁸F-AV45: (E)-4-(2-(6-(2-(2-(2-(18)F-fluoroethoxy)ethoxy)ethoxy)pyridin-3-yl)vinyl)-N-methyl benzenamine; ¹⁸F-AV1451: (7-(6-[18F]fluoropyridin-3-yl)-5H-pyrido[4,3-b]indole, flortaucipir F18; MRA: magnetic resonance angiography.

At the end of the treatment, the patient reported significant improvement in mental well-being, stating, “[My] mental state had reached an unprecedented high level.”

Discussion

This case demonstrates that a combined approach of rTMS and MedDiet may lead to significant cognitive and emotional improvements in an early-stage AD patient with comorbid anxiety. Significantly, the patient discontinued all anti-anxiety medications and expressed high satisfaction with the treatment outcome. The use of rsEEG provided valuable objective evidence of treatment efficacy.

rTMS targeting the DLPFC or PCu are conventional stimulation sites for improving cognition.²² The DLPFC is found critical in cognitive control, decision-making, and emotional regulation.²³ High-frequency stimulation of the DLPFC exerts top-down inhibition on emotion-related regions such as the amygdala, alleviating anxiety and depressive symptoms,²⁴ while modulating neurotransmitter balance (e.g., serotonin, dopamine, GABA) to promote neuroplasticity and neuronal survival.⁷ The PCu is a core component of the default mode network (DMN) and is involved in self-awareness, memory retrieval, and emotional integration.²⁵ rTMS targeting the PCu helps restore DMN connectivity and overall brain synchrony.²⁶ Moreover, recent reviews show that rTMS promotes synaptic plasticity, restores neurotransmitter balance, reduces amyloid and tau buildup, and alleviates neuroinflammation, highlighting its strong potential as a treatment for AD.²⁷ Therefore, combined stimulation of the DLPFC and PCu may synergistically enhance brain network connectivity, improve cognitive function, and alleviate anxiety symptoms.

Furthermore, rTMS has been reported to support medication tapering by attenuating craving intensity and withdrawal symptoms in patients with substance use disorders.^28,29 This mechanism may help explain the observed normalization in our patient's cognitive and emotional assessments after 25 rTMS sessions, potentially facilitating the discontinuation of most psychotropic medications.

rTMS has also shown therapeutic potential when combined with lifestyle interventions, such as low-carbohydrate diets for obesity and aerobic exercise for improving cognition and brain network function in AD.^30,31 The MedDiet played a pivotal role throughout the treatment course. Recognized as a healthy dietary patterns in preventing neurodegenerative diseases, it has been associated with reduced chronic inflammation, limited neurotoxic deposition of Aβ and tau proteins, and provision of antioxidants and neuroprotective nutrients.^32–34 In addition, its rich content of omega-3 fatty acids, folate, and dietary fiber supports neurotransmitter balance and promotes beneficial gut microbiota through the gut–brain axis, thereby mitigating anxiety-related behaviors.¹⁵ Moreover, studies have shown that individuals with the APOE ε4/ε4 genotype are more responsive to the MedDiet, possibly due to its regulatory effects on microglial activation and inflammatory pathways, astrocyte function and lipid metabolism, as well as its influence on insulin resistance and glucose homeostasis.³⁵ This may partially explain the therapeutic efficacy observed in this patient. Thus, by integrating rTMS with MedDiet, we leveraged the complementary benefits of neuromodulation and nutritional intervention, potentially accelerating amyloid clearance, improving both cognitive and emotional outcomes, and reducing medication-related side effects and risks.

rsEEG is a crucial tool not only for epilepsy diagnosis but also for assessing various neurological and psychiatric disorders.³⁶ Our previous study also demonstrated that rsEEG was the most sensitive modality for early AD screening at the subjective cognitive decline stage, outperforming MRI, genomics, and metabolomics approaches.³⁷ The IAF, a stable neurophysiological marker, correlates with cognitive performance and disease severity.³⁸ Faster IAFs are associated with better cognitive performance, while slower IAFs correlate with more severe symptoms and poorer treatment outcomes.³⁹ In this study, the progressive increase in IAF reflects the restoration of brain network synchrony and functional integrity, particularly in the thalamo-cortical and DMNs,⁴⁰ may suggest neural plasticity and significant cognitive recovery, consistent with the improvements in MoCA and MMSE scores. The reduction in beta power may indicate improved mood regulation and the alleviation of depressive and anxious symptoms, as reflected in the HAMA and HAMD score reductions.¹¹ And the relative power spectra of alpha and theta bands, as well as the theta/alpha and theta/beta ratios, may also reflect the patient's cognitive function,^41,42 further supporting rsEEG as a valuable biomarker for tracking disease progression and treatment response.

There are some limitations in this report. Firstly, the patient's extended history of anxiety and prolonged use of high-dose psychotropic medications may have contributed to cognitive decline, complicating the attribution of improvements solely to the interventions. Secondly, due to the patient being away from the local area, immediate cognitive and rsEEG assessments were not conducted following the three rTMS courses and the 20-month MedDiet intervention, which limited the evaluation of the intervention's immediate effects. Furthermore, while both rTMS and the MedDiet have been individually associated with cognitive and emotional benefits, their combined role and underlying mechanisms in this treatment regimen remain uncertain. Future controlled studies with larger sample sizes and comprehensive neurophysiological assessments are necessary to validate these findings and elucidate the distinct contributions and mechanisms of rTMS and the MedDiet in the treatment of cognitive impairment and anxiety in AD.

Conclusion

This case suggests that the integration of rTMS with a MedDiet may offer a safe and individualized strategy for cognitive enhancement and anxiety reduction in early AD. Such multimodal, non-pharmacological approaches could complement existing treatments and provide patients with improved quality of life. Further well-designed clinical trials are needed to confirm these benefits and to clarify the underlying mechanisms.

Footnotes

Acknowledgements

The authors would like to thank the patient and his family for participating.

ORCID iDs

Yumei Liu

Lin Zhu

Zian Pei

Zhifan Zhou

Chongyuan Lian

Xue Shi

Yi Guo

Ethical considerations

This study was reviewed and approved by the Institutional Review Board of Shenzhen People's Hospital (Shenzhen, China) with the approval number: LL-KT-201708001, dated August 14, 2017. This study was conducted in accordance with the Declaration of Helsinki guidelines (chictr.org.cn identifier ChiCTR1800019199). Informed consent was obtained from the patient to publish all images, clinical data, and other data included in the manuscript.

Consent to participate

Written informed consent was obtained from the patient prior to participation in this study.

Consent for publication

Informed consent was obtained from the patient to publish all images, clinical data, and other data included in the manuscript.

Author contribution(s)

Yumei Liu: Conceptualization; Data curation; Writing – original draft.

Lin Zhu: Methodology.

Zian Pei: Methodology.

Zhifan Zhou: Validation.

Xiaolin Su: Investigation.

Huixia Ren: Investigation.

Shuhan Fan: Formal analysis.

Xiaoyong Lan: Investigation.

Chongyuan Lian: Investigation.

Xue Shi: Investigation.

Yi Guo: Formal analysis; Supervision; Writing – review & editing.

Funding

The authors disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This work was supported by the following funds: National Natural Science Foundation of China (82371471); Shenzhen Science and Technology Innovation Commission (KCXFZ20201221173400001; KCXFZ20201221173411032; SGDX20210823103805042).

Declaration of conflicting interests

The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Data availability statement

The authors confirm that the data supporting the findings of this study are available within the article.

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