Abstract

Alzheimer’s Disease (AD) is the most common form of dementia that has symptoms of progressive cognitive decline linked to amyloid-β plaques, tau tangles and disrupted gene regulation. While current treatments slow down the progression of disease, they cannot cure the epigenetic changes. Existing research highlights how music can not only influence in an emotional and psychological way, but it can also benefit the epigenome by altering DNA methylation, histone modifications and microRNA regulation. These studies demonstrate that even a small amount of music can increase dopamine, support synaptic plasticity and regulate stress-related and neuroprotective genes. These mechanisms demonstrate that music therapy can help restore healthy epigenetic patterns and enhance neural resilience in patients with AD. This research paper explores the epigenetic landscape of AD and examines how music therapy can modulate these pathways. We propose music therapy as a treatment for dopamine pathways, stress-regulatory genes and microRNA profiles, offering a potential strategy to reduce AD progression and its risks. 

Introduction to Alzheimer’s Disease and Epigenetics

Alzheimer’s Disease (AD) affects over 55 million individuals worldwide, yet there is no definitive cure, emphasising the urgent need for alternative approaches to combat the detrimental effects of the disease and support those affected. This paper introduces the epigenetic mechanisms that contribute to Alzheimer’s disease and explores how alterations in gene expression influence disease progression. Moreover, the potential of music therapy as a non-invasive treatment alternative is proposed due to its capability to support cognitive health and improve quality of life for patients. Through thorough assessment and research, this article provides a comprehensive understanding of how epigenetic modulation through music could offer promising results within the treatment of Alzheimer’s disease.

Alzheimer’s disease is a neurodegenerative condition and an extremely prevalent form of dementia which results in progressive memory loss, regression in functioning, difficulty processing information and changes in behaviour (Alzheimer’s Association, 2023). AD, in rare cases, can be inherited through genetic mutations as a result of irregular processing of the amyloid precursor protein (APP), which results in the production of amyloid-β peptides that aggregate to form plaques in the brain (Cauwenberghe et al., 2016). However, most instances of developing AD are due to factors such as upbringing, life experiences and epigenetics – changes in gene activity caused by chemical tags and modifications to the chromatin structure without alteration of the DNA sequence (Bird, 2007). Epigenetic changes occur due to factors such as stress, trauma, exposure to harmful substances or diet. It may also be hereditary and pass from parents to offspring across generations (Zannas et al., 2015).

One example of a frequently seen epigenetic modification is DNA methylation, which is when chemical tags attach to DNA and modulate gene expression (Bird & Jaenisch, 2003). An additional example of this is histone modification, which is the change in how tightly DNA is wrapped around proteins within a cell, affecting the accessibility of the genes (Kouzarides, 2007). These epigenetic changes concerning our DNA are constantly occurring and normal; however, in some cases, these changes can increase the vulnerability and risk of diseases, including cancer, type 2 diabetes, schizophrenia and Alzheimer’s disease (Feinberg, 2018).

Certain epigenetic patterns within a person’s DNA affect their vulnerability towards AD – a result of the epigenetic patterns being disrupted (De Jager et al., 2014). For example, genes that are protecting brain cells may be switched off while genes that induce inflammation may be switched on, together leading to cognitive and memory decline over time.

Understanding Alzheimer’s Disease

Alzheimer’s disease is a chronic neurodegenerative disorder compromising cognitive function, memory, visuospatial skills and the ability to perform daily tasks. Representing the majority of dementia cases, AD is responsible for approximately 70% of cases worldwide (Nikolac Perkovic et al., 2021). From a pathological standpoint, it is defined by extracellular amyloid-β (Aβ) plaques which arise from abnormal beta-secretase (BACE1) and gamma-secretase processing in the amyloid precursor protein (APP) embedded in the neuronal membrane. These plaques interfere with synaptic signalling and can trigger neuroinflammation. Alongside the plaques, neurofibrillary tangles are composed of hyperphosphorylated tau proteins that contribute to cell death and further breakdown of synapse function. Most instances of AD are sporadic and manifest after the age of 65, known as Late Onset Alzheimer’s Disease (LOAD), making up over 95% of overall cases and arising from genetic variability, environmental exposures and epigenetic regulation (Nikolac Perkovic et al., 2021; Liu et al., 2018). In contrast to the rare early-onset familial forms linked to pathogenic mutations in APP, PSEN1 and PSEN2, the predominance of late-onset cases emphasises the urgency of probing regulatory layers that lie beyond the DNA sequence, with a particular focus on epigenetic modulation.

The Epigenetic Landscape of Alzheimer’s Disease

Increasing evidence indicates that AD arises not only from genetics and ageing, but from epigenetic factors. The epigenome, which controls gene activity without changing the DNA sequence, responds to a variety of influences including ageing, stress, diet, trauma and exercise and translates these signals into alterations of brain circuits fundamental to memory, learning and neuronal resilience Such epigenetic remodelling is increasingly recognised as a key driver of AD progression (Liu et al., 2018; Nikolac Perkovic et al., 2021).

In contrast to a genetic mutation’s fixed nature, epigenetic marks are malleable and, theoretically, reversible. Due to this flexibility, they can be targeted for therapeutic intervention; medications, lifestyle changes, stress reduction and even exposure to music have all been shown to have the ability to alter the epigenome. Additionally, preliminary research indicates that these epigenomic changes can be identified well before memory impairments, making them potential biomarkers for early intervention and a foundation for preventative measures (Liu et al., 2018).

The epigenetic landscape of AD provides more than just information about the illness – it creates new opportunities for non-invasive, customised treatments. The following sections will explore in detail how specific epigenetic mechanisms are altered in AD and how reversing these changes may slow or halt disease progression.

DNA Methylation and Hydroxymethylation in AD

DNA methylation, which involves adding a methyl group to cytosine bases at CpG islands, is important for modifying cellular processes like gene expression and silencing repetitive sequences to maintain cellular identity in the brain. Within the neurons, DNA methylation regulates synaptic activity, neurogenesis and memory formation. In the context of AD however, methylation changes contribute to the disturbance of cellular processes and increase the risk of neuroinflammation and neurodegeneration (Nikolac Perkovic et al., 2021; Liu et al., 2018).

Studies have identified altered methylation states in numerous AD-related genes. One change is the hypomethylation of the promoter region of the APP gene which leads to increased expression of the amyloid precursor protein, contributing to the overproduction of amyloid-β (Aβ) proteins (Liu et al., 2018). Another associated change is the abnormal methylation of BDNF, a gene that is important for memory retention and long-term potentiation (LTP) which is associated with the decline in cognitive functions. The elevation of methylation at certain BDNF promoter regions is known to suppress its expression, which diminishes the capacity of the brain to adapt and endure damage (Nikolac Perkovic et al., 2021).

Notably, ANK1 is hyper- or hypomethylated in AD in regions such as the hippocampus and the entorhinal cortex which highly contribute to the AD pathology. It is also one of the most consistently epigenetically altered genes in brains with Alzheimer’s. Liu and colleagues have suggested it is associated with the cytoskeletal changes and the hyperactive inflammatory response observed in AD. TREM2, a gene associated with microglial activity and the regulation of immune functions, also has risk associated with altered methylation changes which dysregulate the brain’s response to the pathogenic Aβ plaques.

Epigenetic regulation of the brain can also be further complicated by the presence of hydroxymethylation, which is the process of converting 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). It is 5hmC that is enriched in the neuron and marks transcriptionally active genes, particularly the ones associated with learning and memory. AD is characterised by the loss of 5hmC globally, particularly in genes involved in synaptic activity, mitochondrial functions and the maintenance of the neurons (Nikolac Perkovic et al., 2021). The reduction of this mark leads to the inability to activate necessary genes essential for the neuronal health and survival.

Importantly, the alterations of methylation and hydroxymethylation do not affect the entire brain uniformly. These changes occur in specific patterns that correlate with particular regions of the brain and the stage of disease. This suggests a breakdown of the brain’s epigenetic control in a spatially-structured and progression-dependent manner, which may allow for targeted treatments in specific regions of the brain.

Histone Modifications and Chromatin Remodelling

DNA wraps around histone proteins to form chromatin. Chemical modifications to these histones, such as acetylation and methylation, regulate how accessible particular genes are. This type of regulatory imbalance results in widespread gene silencing in AD. In AD, histone deacetylases (HDACs), especially HDAC2 and HDAC6, are often overactive. This overactivity results in HDACs condensing chromatin, silencing genes that aid synaptic plasticity, memory and cellular repair (Liu et al., 2018). 

Inflamed HDAC2 is problematic in AD because it silences key genes responsible for learning and memory. In brain regions affected by AD, elevated levels of HDAC2 have been recorded. In disease models, blocking HDAC2 was shown to enhance chromatin accessibility to plasticity genes and improve cognitive function. Further, HDAC6 contributes to the aggregation of tau protein and impairs axonal transport. It has been shown that the inhibition of HDAC6 decreases tau toxicity and enhances neuronal communication.

Besides acetylation, alterations in acetylcholinesterase AD may also interfere with methylation and other histone changes, impacting immune response and stress management genes – specifically, FKBP5. The potential to modify histones is a therapeutic target of interest. Treatments that disrupt the balance of histone acetylation, such as HDAC inhibitors, could restore normal gene expression and mitigate neurodegeneration in AD.

Dysregulation of Micro-RNAs and Non-Coding RNA

MicroRNAs, also known as miRNAs, are a type of small non-coding RNA molecules responsible for post-transcriptionally regulating gene expression by either degrading or inhibiting specific mRNAs. In AD, many miRNAs are expressed abnormally which alters genes related to inflammation, neurogenesis and homeostasis of proteins. In AD, miR-132 is often downregulated, which is maladaptive as it downregulates memories and synaptic plasticity. Other miRNAs like miR-23a, which are also neuroprotective and are related to stress responses, can also worsen neurodegenerative changes if their expression is perturbed (Navarro, 2023). Several of these modified miRNAs have been found to circulate in blood and cerebrospinal fluid, indicating potential as non-invasive, early diagnostic markers (Liu et al., 2018).

Mitoepigenetics: A New Frontier

Numerous studies on the epigenetics of AD have focused on the regulation of nuclear DNA; however, current research indicates that mitochondrial epigenetics, or “mitoepigenetics”, may significantly influence the disease pathology, a role previously underestimated (Nikolac Perkovic et al., 2021). Mitochondria are responsible for a number of important processes, such as energy production, calcium homeostasis and apoptosis regulation, especially neurons. These functions are important  to the brain, given its high energy requirements. Dysfunction of mitochondria can be catastrophic, leading to cognitive impairment and dementia (Nikolac Perkovic et al., 2021).

In AD, there are several reported mitoepigenetic abnormalities. These are a decrease in mitochondrial DNA (mtDNA) copy number, alteration in mitochondrial transcription and changes in methylation marks in the mitochondrial DNA (mtDNA) genome (Nikolac Perkovic et al., 2021). Such changes lead to impairment in mitochondrial gene expression and the synthesis of ATP, increasing oxidative stress and causing the accumulation of reactive oxygen species (ROS), damaging neurons and worsening amyloid and tau pathology. Epigenetic deregulation in mitochondria could inhibit the process of mitophagy, the removal of damaged mitochondria, and thus, speed up cellular ageing and degeneration  (Nikolac Perkovic et al., 2021).

Although research on mitoepigenetics in AD is still in its early stages, its potential is substantial. The control of mtDNA epigenetics creates a possibility for specific environmental interventions, changes or epigenetic suppression. It may be possible to design therapies that support neuronal resilience by restoring proper methylation of mtDNA or by enhancing mitochondrial biogenesis and subsequently slow down the progression of the disease. With time, mitoepigenetics could serve not just as a biomarker of a disease’s severity, but also as a new front in the fight against AD.

With the progression of research on AD, the disease’s epigenetic aspects such as nuclear DNA methylation, histone modification and even mitochondrial epigenetics are coming to light. In turn, it becomes increasingly evident that gene regulation is deeply influenced by environmental and lifestyle factors. This recognition has sparked interest in non-pharmacological interventions that can reshape epigenetic patterns to support brain health. Music therapy is one such intervention that has become popular and can be easily accessed. As epigenetic marks are dynamic and responsive to external stimuli, music may represent a powerful tool for reactivating key genes involved in neuroplasticity, memory and cellular resilience. The following section explores how musical engagement can influence epigenetic mechanisms at the molecular level and potentially slow or prevent cognitive decline in individuals at risk of or living with AD.

Music Therapy: The Future of Epigenetic Treatment

As music therapy affects prevalent areas of the brain linked to memory, movement, emotions and language, it is quickly becoming a viable approach to addressing challenges that emerge as a result of neurodegenerative conditions (Sarkamo et al., 2014). Music can act as a powerful means of connection for AD patients due to their declining ability to communicate with words and memories. In many instances, AD and dementia patients are able to recall song lyrics and tunes which were otherwise inaccessible due to memory loss (Bleibel et al., 2023).

The use of music therapy in combatting neurodegenerative challenges promotes feelings of connection and positivity while diminishing stress, together acting as a catalyst to improve the daily lives of AD patients (Thompson et al., 2024). The effects of music go beyond emotional and psychological impacts; increased evidence shows that music also affects gene expression which is the process by which genes are turned on or off. For example, studies have shown that listening to music can change the levels of microRNAs which assist in regulating gene activity and are important to brain health (Kanduri et al., 2024). 

This connection between music and gene activity raises the possibility that music could make a macro impression on genes and subsequently treat diseases such as AD epigenetically. For example, AD patients often show increased methylation of protective genes; if music could be used to reverse the harmful effects of gene methylation, the protective genes – such as KL, which reduces inflammation (Dubnov et al., 2024) and APOE ε2, which lowers risk of AD and delays onset – could be be reactivated (Liu et al., 2013). This demonstrates how music therapy could be a valuable treatment for neurodegenerative diseases, simultaneously improving mood, memory and recall (Navarro et al., 2023).

The use of music within treatment is further supported as it is non-invasive, safe and accessible for all patients. AD poses many challenges for patients and family due to its mental, social and emotional toll on everyone affected. The current available treatments may slow down the damaging process of AD, but do not completely cure the disease, which is why the exploration of alternative pathways of treatment, such as epigenetic changes as a result of music therapy, is so important (Livingston et al., 2020).

Music’s Role in Enabling Positive Epigenetic Alterations

With this newfound epigenetic knowledge, it is clear that alterations in gene expression positively guide any disruption of the body’s homeostasis back to normal. These epigenetic marks, such as DNA methylation, histone modifications and miRNA alterations, help our bodies in the response and adaptation to environmental factors and stress (Navarro, 2023). This is especially vital for genes that handle neuroplasticity and stress response, as impaired epigenetic mechanisms can accelerate cognitive decline (Zannas et al., 2015).

When these mechanisms respond accurately, the brain maintains its flexibility and ability to rapidly recover from any disruption. However, any discrepancies to these processes can make it more challenging for neurons to adapt in times of distress. This challenge is significant for AD as problems with neuroplasticity and stress response can speed up the process of cognitive decline. Therefore, there is much anticipation for the role of music therapy in aiding the prevention of this decline, due to the ways in which it could change epigenetic patterns in the brain (Kanduri et al., 2015; Nair et al., 2021).

Music-Induced Changes in Gene Expression

A 2015 study found that blood gene expression was altered after only one 20-minute session of listening to Mozart’s Violin Concerto No. 3. The amount of the gene expression response, however, was found to be greater in participants who had prior musical training compared to those who did not. Through blood samples and RNA sequencing, it was found that many of these altered genes were responsible for pathways such as dopamine signalling, synaptic functions and protection of neurons. The synaptic vesicles’ release and recycling, along with receptor activity, which are controlled by dopamine, help to make up a healthy memory. Dopamine enables attention, learning and synaptic plasticity, which are vital for strengthening and creating a healthy brain. The pathways that strengthen neurons against damage aid against neuron degeneration, which occurs in patients with AD and eventually leads to memory loss and confusion. These alterations were even more evident in people with prior musical training, highlighting that lifelong music engagement could make the brain more positively responsive. As dopamine and synaptic activity are some of the first systems disrupted in AD, the way in which music strengthens these vital pathways demonstrates real potential for slowing down or offsetting damaging symptoms from AD (Kanduri et al., 2015).

Music’s Effect on micro-RNA Regulation

MicroRNAs can also be targeted to strengthen brain functions, such as memory formation and recovery from stress. Music’s role in altering this epigenetic mark can impact these two major areas that are significantly affected by AD.

In a 2021 study, it was found that after 20 minutes of listening to classical music, multiple significant miRNAs were largely regulated. Specifically, the miR-132 was significantly regulated, which encourages learning, memory and neuron growth. Additionally, this miRNA helps to prevent the overproduction of the tau protein within neurons, which agglomerates as a result of obtaining AD. Other miRNAs are also crucial for the health of the brain, such as the miR-23a, which protects neurons from any damages that may occur as a result of stress. In AD, many of these miRNAs are dysregulated and ultimately negatively affect the body and the brain. The positive results from the study support the role that music can play in altering these miRNAs to re-establish healthy patterns (Nair et al., 2021).

Music Preventing Altered Gene Patterns in Cognitive Decline

Rather than performing a study on healthy individuals, Gómez-Carballa along with others tested the effects of music on individuals with symptoms of neurological decline. Participants in this study, who were already affected with mild cognitive impairment (MCI) or AD, listened to 20 minutes of personalised playlists and were studied for the results. 

The music was found to have promoted autophagy, which removes damaged proteins such as tau, which can clump up in neurons and worsen AD symptoms. Additionally, vesicle transport was shown to increase the signals sent between neurons due to the upregulation of certain genes linked to neurotransmission, which normally is reduced in AD. These effects from the music led to this sudden shift of gene activity which was the opposing results of the normal AD patterns. These results suggest that music can influence and shift the brain towards healthier patterns for this disease, even after the symptoms have progressed (Gómez-Carballa et al., 2023).

Sensogenomics

Sensogenomics is a field of study which highlights how highly sensory experiences can alter the brain at a molecular level, which very strongly correlates to music and its effects on gene expression. It is highlighted that AD is not only memory loss, but is also about extensive alterations in gene expression and epigenetic patterns. If music can influence these pathways, it could be used alongside other treatments to strengthen the brain through increasing its neuroplasticity and ultimately delaying AD cognitive symptoms. Although it is a relatively new area of study, multiple studies provide evidence to support the positive findings and encourage further research to aid those who suffer from AD (Navarro, 2023).

Stress Epigenetic Modulation Through Music

Chronic stress is a common risk factor for AD and its consequences can include negative marks on the epigenome. A study investigated these specific epigenetic modifications through studying rodents’ responses to repeated stress for four weeks. DNA methylation was found upstream of the BDNF gene, which is a vital neuroplasticity factor (Nair et al., 2021). This hypermethylation, with the reduced expression of BDNF, is detrimental for AD patients as this molecule is critical for neuron survival. In some cases, these harmful epigenetic marks can even be passed down to future generations through epigenetic inheritance, which ultimately increases AD risk throughout generations. However, music has been shown to lower cortisol levels in the body and is linked to the upregulation of specific miRNAs, such as miR-132, which promote learning (Nair et al., 2021). Thus, these factors uniting to strengthen neuroprotective genes create a high possibility of the direct reversal of negative stress-related epigenetic modifications.

‘Healing with Harmony’: A Real-World Application

‘Healing with Harmony’ is a project created by two sisters, Luciana and Daniela Vargas, who perform as a violin duo for underserved communities, hospitals and nursing homes. Offering their music completely free, they aspire to provide healing, hope and joy to everyone they encounter. Their performances provide a real-world example of how anyone can be an agent of change by spreading healing through music (Healing with Harmony, 2025).

Through 10+ years of performing in nursing homes, they have witnessed people living with AD remember songs they have not heard in decades. Some sing along, others laugh or cry and many share stories about past memories which were triggered by the music. These reactions align closely with the research highlighting that music can increase dopamine, a neurotransmitter that is vital for motivation, attention and memory, which are all compromised in AD. Through these performances, the sisters act as “transfers” of dopamine, helping to boost mood and engagement in their listeners while also strengthening their own brain processes by playing the violin. The moments they create often appear to unlock neural pathways that AD disrupts, temporarily restoring connections that allow people to remember, feel and communicate.

‘Healing with Harmony’ demonstrates that the scientific principles found in laboratory studies are not confined to research settings and can come alive in everyday acts of sharing music. Whether in a hospital room or in a nursing home lounge, music has the power to revive memories, stimulate dopamine release and potentially strengthen the same brain pathways that are threatened in AD.

Proposal of Studies and Treatments for Epigenetically Inherited Alzheimer’s Using Music Therapy

In the field of AD and epigenetics, music plays an important role. It can induce beneficial changes associated with neuroplasticity, neuronal protection and stress regulation. For individuals at risk of AD through epigenetic inheritance, adverse gene expression patterns – such as aberrant methylation of stress-regulatory genes like FKBP5 – can be passed down across generations (Zannas et al., 2015).

Building on the above evidence that music is able to benefit people with AD, the goal for this paper is to develop and test music-based treatments and propose new strategies. While existing findings are promising, coming up with solutions that specifically aid AD may make treatment more effective. The creation of such treatments is particularly useful for people affected by more damaging forms of epigenetic inheritance, which can result in harmful gene expression patterns. By addressing these patterns, future generations may also be protected from inheriting maladaptive epigenetic traits.

Targeted Music-Based Epigenetic Therapy

Music-based epigenetic therapy uses personalised music therapy to create beneficial epigenetic changes in the brain. Specific pieces, such as Vivaldi’s Four Seasons which has an upbeat and lively tone, can influence gene expression that supports dopamine signalling, synaptic function and neuron protection (Kanduri et al., 2015). It can also regulate key microRNAs, which are vital for memory, neuron survival and preventing harmful tau protein build-up (Nair et al., 2021).

AD disrupts dopamine pathways, reduces brain plasticity and alters microRNAs, which are critical for brain health (Kanduri et al., 2015; Nair et al., 2021). Targeting these mechanisms through music therapy can restore and provide healthier gene activity while also improving neuron communication and protecting against cell damage (Kanduri et al., 2015). As previously mentioned, even short music sessions have been shown to boost dopamine-related processes, enhance attention and memory and regulate microRNAs that protect neurons. These benefits may be even greater in individuals with prior musical experience (Kanduri et al., 2015).

In targeted music-based epigenetic therapy, participants would engage in 20-30 minutes of daily listening to classical music, as this has been shown to stimulate dopamine activity and beneficial microRNA regulation (Nair et al., 2021). People with any kind of musical training, whether singing or playing an instrument, could participate actively, potentially leading to stronger results (Kanduri et al., 2015). Blood tests for gene and microRNA changes, cognitive testing and quality-of-life surveys would be used to measure effects before and after the intervention. The hoped-for outcomes would include improved dopamine signalling, balanced Alzheimer’s-affected microRNAs, better memory scores and lower stress biomarkers (Nair et al., 2021; Zannas et al., 2015).

Micro-RNA Focused Therapeutic Applications

MicroRNA focused therapeutic applications use music therapy to restore healthy levels of microRNAs. Research shows that miR-132 and miR-23a can be positively regulated by listening to classical music with dynamic variation and richness and strong sounds in harmonies (Nair et al., 2021). In AD, miRNAs are disturbed, damaging neurons and accelerating memory loss. Music therapy can help normalise these levels, promoting learning, stress protection and cell survival, which may allow for the delay of symptom progression and improvement of daily cognitive function.

Participants suffering from AD or mild cognitive impairment would participate in anywhere from 20-30 minutes of music sessions, similar to targeted music-based epigenetic therapy. However, the music for this approach is personalised. The participants are able to pick which songs they listen to. Progress would be tracked through blood tests for miRNA changes, cognitive testing and stress assessments, which we hope would lead to restored miRNA balance, improved memory scores and greater resilience to stress.

Treatments and Targets

Though similar, the above treatments have different epigenetic targets. The targeted music-based epigenetic therapy treatment aims to collect DNA methylation in many forms, like dopamine pathway genes and FKBP5 stress-regulation. The microRNA focused therapeutic applications approach focuses on the miR-132 and miR-23a regulations, as these are what control the gene expression.

The above treatments and targets would allow for the collection of data on responsible epigenetic mechanisms and could prove the connection between AD and music, changing the way the disease progresses in the future.

Conclusion

Music not only enriches our emotional lives, but can also induce biological changes that protect and strengthen the brain. Listening to music can increase dopamine (the “motivation and memory” chemical), improve how brain cells communicate with each other, protect neurons from damage and even fix tiny regulators called microRNAs that help control learning, memory and stress. As these systems break down over time in Alzheimer’s disease, restoring them is essential.

Studies demonstrate that even short periods of music-listening can improve gene expression patterns associated with learning, memory and neuronal protection. These effects are strongest in people with musical training, but are also noticeable in people who are experiencing cognitive decline. Music therapy has been shown to reverse the gene activity that is related to cognitive decline, promote removal of toxic proteins and aid in communication between brain cells. Additionally, sensogenomics has the potential to act as a preventative measure and a complementary treatment for those with an epigenetic predisposition for AD. Stress-related epigenetic changes, such as harmful methylation patterns in the FKBP5 gene, can also be impacted through music therapy, helping to reduce cortisol levels and promote relaxation. 

While further research is needed, music therapy provides an opportunity to preserve memory, foster emotional connection and improve the overall quality of life. In the fight against AD, music can be a powerful medicine.

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