What Is Cellular Senescence and How Does It Affect Hair Growth?

10 min read

February 19,2025

LONGEVITY

What Is Cellular Senescence and How Does It Affect Hair Growth?

10 min read

February 19,2025

LONGEVITY

If your hair isn't growing like it used to, it could be due to cellular senescence, one of the key hallmarks of aging. This biological process affects not only your skin but also your scalp (which is skin, too!), disrupting the natural hair growth cycle.Senescent cells accumulate in most tissues of the body with age, including the skin and hair follicles, leading to dysfunction over time. This accumulation contributes to visible signs of aging, such as wrinkles, hair greying, and hair thinning. Scientists, including our own, have discovered that reducing senescence in tissues like hair follicles and skin can reverse aspects of the aging process, leading to visible improvements [1,2,3,4] Even more promising, molecules like our patented OS-01 peptide have been shown to reduce senescence in hair and skin models, offering an accessible way to counteract the visible effects of aging by targeting cellular aging. [1,5]

01

How Cellular Senescence Impacts Hair Growth

Hair growth relies on a well-orchestrated cycle of four phases: anagen (growth), catagen (transition), telogen (resting), and occasionally kenogen (lag).[6] While the length of each phase varies, most hair cycles last three to seven years. Between cycles, most of the hair follicle must regenerate to produce a new hair that replaces the one shed. This process is guided by the dermal papilla (DP) at the base of each follicle. Acting as tiny conductors, DP cells initiate and regulate the growth phase by signaling surrounding cells to proliferate and differentiate, ultimately forming a new hair. They also influence the hair’s size, shape, and color. [6]

01

How Cellular Senescence Impacts Hair Growth

Hair growth relies on a well-orchestrated cycle of four phases: anagen (growth), catagen (transition), telogen (resting), and occasionally kenogen (lag).[6] While the length of each phase varies, most hair cycles last three to seven years. Between cycles, most of the hair follicle must regenerate to produce a new hair that replaces the one shed. This process is guided by the dermal papilla (DP) at the base of each follicle. Acting as tiny conductors, DP cells initiate and regulate the growth phase by signaling surrounding cells to proliferate and differentiate, ultimately forming a new hair. They also influence the hair’s size, shape, and color. [6]

Among the cells responding to DP signals, outer root sheath cells (ORSCs) play a key role in the anagen phase and the thickness and stability of hair. Within the outer root sheath, a structure called the bulge houses stem cells essential for hair growth, while the rest of the outer root sheath helps guide these cells to the proper locations for growth. [7, 8] Lining the follicle’s outer layer, ORSCs also support the structural integrity of the follicle. [9]

Diagram from https://www.nature.com/articles/ng0306-273

As you age, follicles atrophy, and hairs become thinner and less dense.[10] Emerging research suggests this decline may be linked to the buildup of senescent dermal papilla cells, making them less effective conductors and impairing their ability to initiate and foster healthy hair growth. [4,10,11] Senescence of other hair follicle cells, particularly stem cells, has also been implicated with hair thinning and loss. [11] Additionally, a decrease in senescence has been associated with an increase in ORSC viability and proliferation. [9]Senescent cells are like bad neighbors—they not only stop being productive members of their community but also secrete inflammatory signals called senescence-associated secretory phenotype (SASP) that damage neighboring healthy cells and create a pro-inflammatory environment, disrupting tissue function. When cells in hair follicles become senescent, hair follicle regeneration is impacted.[4] This chain reaction contributes to certain types of hair thinning and hair loss.[3]

Diagram from https://www.nature.com/articles/ng0306-273

As you age, follicles atrophy, and hairs become thinner and less dense.[10] Emerging research suggests this decline may be linked to the buildup of senescent dermal papilla cells, making them less effective conductors and impairing their ability to initiate and foster healthy hair growth. [4,10,11] Senescence of other hair follicle cells, particularly stem cells, has also been implicated with hair thinning and loss. [11] Additionally, a decrease in senescence has been associated with an increase in ORSC viability and proliferation. [9]Senescent cells are like bad neighbors—they not only stop being productive members of their community but also secrete inflammatory signals called senescence-associated secretory phenotype (SASP) that damage neighboring healthy cells and create a pro-inflammatory environment, disrupting tissue function. When cells in hair follicles become senescent, hair follicle regeneration is impacted.[4] This chain reaction contributes to certain types of hair thinning and hair loss.[3]

02

The Role of Senescence in Different Types of Hair Loss

While there are various causes of hair loss, three of the most common types of hair loss – pattern balding, age-related thinning, and stress-induced hair loss – are linked to cellular senescence. [10,12,13,14,15] Additionally, less commonly experienced hair loss from chemotherapy is also linked to senescence. [7]

Pattern Balding

Characterized in men by hair loss around the temples and crown of the head, pattern balding is predominantly driven by androgen-mediated mechanisms, particularly the conversion of testosterone into dihydrotestosterone (DHT) by 5α-reductase, which can begin as early as your 20s.[12] This process causes hair follicles to gradually shrink, called follicle miniaturization, in predictable patterns, converting terminal hairs (or thick, pigmented) hairs into finer vellus hairs that eventually atrophy.[12,16]One of the most common types of hair loss, pattern balding affects about half of all men by age 50, [16] with up to 80% experiencing it throughout their lifetime.[13] While less common, many women are also affected, with 40% showing signs of pattern balding by age 70 and 50% being affected throughout their lifetime.[16,17]Interestingly, hormone levels like testosterone and DHT are known to decrease with age, while prevalence increases with age, prompting scientists to believe that pattern baldness may also be influenced by an aging process: cellular senescence. They have found that while aging or senescent cells don’t directly cause pattern baldness, they’re a contributing factor that can exacerbate hair loss over time.[12] Here’s how:Research shows that dermal papilla cells (DPCs) in balding areas tend to experience premature senescence and display a higher level of senescence markers like IL-6 and p16. [10,14] Additionally, stems cells in the outer root sheath are diminished in balding scalp and might contribute to miniaturization and delay hair follicle regeneration [8, 18] This indicates that dysfunction associated with cellular senescence likely contributes to hair follicle miniaturization in pattern balding. [13]. Additionally, androgens may increase cellular stress responses by inducing or exacerbating oxidative stress and/or DNA damage–two factors that increase senescence.[13,19]

02

The Role of Senescence in Different Types of Hair Loss

While there are various causes of hair loss, three of the most common types of hair loss – pattern balding, age-related thinning, and stress-induced hair loss – are linked to cellular senescence. [10,12,13,14,15] Additionally, less commonly experienced hair loss from chemotherapy is also linked to senescence. [7]

Pattern Balding

Characterized in men by hair loss around the temples and crown of the head, pattern balding is predominantly driven by androgen-mediated mechanisms, particularly the conversion of testosterone into dihydrotestosterone (DHT) by 5α-reductase, which can begin as early as your 20s.[12] This process causes hair follicles to gradually shrink, called follicle miniaturization, in predictable patterns, converting terminal hairs (or thick, pigmented) hairs into finer vellus hairs that eventually atrophy.[12,16]One of the most common types of hair loss, pattern balding affects about half of all men by age 50, [16] with up to 80% experiencing it throughout their lifetime.[13] While less common, many women are also affected, with 40% showing signs of pattern balding by age 70 and 50% being affected throughout their lifetime.[16,17]Interestingly, hormone levels like testosterone and DHT are known to decrease with age, while prevalence increases with age, prompting scientists to believe that pattern baldness may also be influenced by an aging process: cellular senescence. They have found that while aging or senescent cells don’t directly cause pattern baldness, they’re a contributing factor that can exacerbate hair loss over time.[12] Here’s how:Research shows that dermal papilla cells (DPCs) in balding areas tend to experience premature senescence and display a higher level of senescence markers like IL-6 and p16. [10,14] Additionally, stems cells in the outer root sheath are diminished in balding scalp and might contribute to miniaturization and delay hair follicle regeneration [8, 18] This indicates that dysfunction associated with cellular senescence likely contributes to hair follicle miniaturization in pattern balding. [13]. Additionally, androgens may increase cellular stress responses by inducing or exacerbating oxidative stress and/or DNA damage–two factors that increase senescence.[13,19]

Age-Related Thinning

Age-related thinning, sometimes called senescent alopecia (SA), is associated with diffuse thinning across the scalp after the age of 50-60. [20,21] Most experts agree the primary attributes of age-related thinning include a decrease in hair diameter and shorter hair (due to a reduction of time spent in the anagen phase and an increase in the telogen phase), commonly accompanied by greying.[22] Some other experts also include hair follicle miniaturization as a characteristic, though there is some debate.[12] Unlike pattern balding, age-related thinning isn’t linked to androgens. [12] Some researchers now believe this progressive decline in hair follicle regeneration with age is due to senescence in dermal papilla cells (DPCs), which can be induced by systemic senescence or aging, oxidative stress, and other damage to the hair follicle cells.[10,12] Additionally, proliferation of ORSCs were seen to decrease in aging follicles which contributes to delayed anagen, along with a less stable follicle. [23] This indicates that senescence-induced dysfunction in DPCs and ORSCs may further exacerbate age-related hair thinning by impairing the follicle's ability to sustain prolonged growth phases.Although the term senescent alopecia (SA) is not widely acknowledged as a distinct medical condition, it has been commonly cited that progressive hair thinning is associated with aging regardless of family history and may constitute its own condition.[12] This is supported by the fact that patients with progeria, who have genetically programmed premature senescence exhibit diffuse hair loss.[12] Here are some key features to help you spot the signs of age-related thinning:

Reduced hair thickness: Research shows that hair follicle aging is featured by a progressive decline in hair shaft diameter, resulting in thinner hair.[10] This may be due to a reduction in activity of ORSCs since the more actively ORSCs proliferate, the larger the hair shaft diameter will be. [8]
Less density: Research also shows that hair follicles atrophy with age which can even cause a gradual loss of follicles, resulting in decreased density as less hairs are in the anagen phase. [10]
Prolonged resting periods: Aged hair follicles tend to spend more time in the telogen (resting) phases, delaying regrowth.[10]

Age-Related Thinning

Age-related thinning, sometimes called senescent alopecia (SA), is associated with diffuse thinning across the scalp after the age of 50-60. [20,21] Most experts agree the primary attributes of age-related thinning include a decrease in hair diameter and shorter hair (due to a reduction of time spent in the anagen phase and an increase in the telogen phase), commonly accompanied by greying.[22] Some other experts also include hair follicle miniaturization as a characteristic, though there is some debate.[12] Unlike pattern balding, age-related thinning isn’t linked to androgens. [12] Some researchers now believe this progressive decline in hair follicle regeneration with age is due to senescence in dermal papilla cells (DPCs), which can be induced by systemic senescence or aging, oxidative stress, and other damage to the hair follicle cells.[10,12] Additionally, proliferation of ORSCs were seen to decrease in aging follicles which contributes to delayed anagen, along with a less stable follicle. [23] This indicates that senescence-induced dysfunction in DPCs and ORSCs may further exacerbate age-related hair thinning by impairing the follicle's ability to sustain prolonged growth phases.Although the term senescent alopecia (SA) is not widely acknowledged as a distinct medical condition, it has been commonly cited that progressive hair thinning is associated with aging regardless of family history and may constitute its own condition.[12] This is supported by the fact that patients with progeria, who have genetically programmed premature senescence exhibit diffuse hair loss.[12] Here are some key features to help you spot the signs of age-related thinning:

Reduced hair thickness: Research shows that hair follicle aging is featured by a progressive decline in hair shaft diameter, resulting in thinner hair.[10] This may be due to a reduction in activity of ORSCs since the more actively ORSCs proliferate, the larger the hair shaft diameter will be. [8]
Less density: Research also shows that hair follicles atrophy with age which can even cause a gradual loss of follicles, resulting in decreased density as less hairs are in the anagen phase. [10]
Prolonged resting periods: Aged hair follicles tend to spend more time in the telogen (resting) phases, delaying regrowth.[10]

Stress-Induced Hair Loss

Stress doesn’t just impact your mood—it also affects your hair follicles.[22] Emerging research underscores the critical role of stress-induced cellular senescence in inhibiting hair growth and ultimately causing hair loss.[22] While direct evidence linking specific stress-induced hair loss conditions, such as telogen effluvium, requires further study, cellular senescence represents a promising target for stress-induced hair loss. Stress triggers the release of hormones from the adrenal gland, which can induce cellular senescence in peripheral tissues, including skin and hair.[15] Specifically, corticotropin-releasing hormone (CRH) has been shown to drive senescence in hair follicle cells, disrupting their growth cycle by prompting an early exit from the anagen (growth) phase.[15] Interestingly, during pregnancy and leading up to labor, concentrations of CRH progressively increase and can reach 1,000 to 10, 000 times of that found in the non-pregnant individuals. [24] While the cause of postpartum hair loss is primarily cited as a drop in estrogen, it is possible that an increase in CRH may also play a role and more research should be conducted to explore this connection.

Stress-Induced Hair Loss

Stress doesn’t just impact your mood—it also affects your hair follicles.[22] Emerging research underscores the critical role of stress-induced cellular senescence in inhibiting hair growth and ultimately causing hair loss.[22] While direct evidence linking specific stress-induced hair loss conditions, such as telogen effluvium, requires further study, cellular senescence represents a promising target for stress-induced hair loss. Stress triggers the release of hormones from the adrenal gland, which can induce cellular senescence in peripheral tissues, including skin and hair.[15] Specifically, corticotropin-releasing hormone (CRH) has been shown to drive senescence in hair follicle cells, disrupting their growth cycle by prompting an early exit from the anagen (growth) phase.[15] Interestingly, during pregnancy and leading up to labor, concentrations of CRH progressively increase and can reach 1,000 to 10, 000 times of that found in the non-pregnant individuals. [24] While the cause of postpartum hair loss is primarily cited as a drop in estrogen, it is possible that an increase in CRH may also play a role and more research should be conducted to explore this connection.

03

The Future of Hair Loss Treatment: Targeting Senescence

Due to the association of senescence and multiple types of hair loss, many experts believe the next generation of hair loss treatments will be focused on combating senescence, the aging process that compromises scalp health and follicle function.[3,4] By targeting senescence in dermal papilla cells (DPCs), outer root sheath cells (ORSCs), and hair follicle stem cells (HFSCs), reducing harmful inflammatory SASP, and combating oxidative stress, these cutting-edge therapies have the potential to address the root causes of follicular aging to restore the vitality of your hair:

Senolytics: Senolytics are a class of molecules that selectively target senescent cells and cause them to undergo apoptosis (programmed cell death), helping minimize their harmful effects on the body. Research shows that senolytic treatments, like quercetin and dasatinib, can mitigate their negative impact on the hair follicle microenvironment, presenting a promising strategy for restoring hair growth and combating hair loss by reducing senescent cells in the hair follicle.[4] Other researchers have found that senolytic treatment could partially reverse age-related hair loss in both normal aged mice, as well as genetically fast-aging mice by restoring tissue homeostasis within the hair follicle and promote hair growth.[3]
Senomorphics: Senomorphic molecules target senescence by reducing the expression of inflammatory factors called SASP from senescent cells, preventing their spread. Researchers suspect that reducing SASP-driven inflammation improves the regenerative environment, supporting the recovery of hair follicle activity and promoting new hair growth.[3] Therapies like rapamycin and metformin have shown promise for their potential to suppress damaging inflammatory factors such as IL-6, which could mitigate hair follicle damage.[13] Additionally, our OS-01 peptide has been shown to act as a senomorphic and shows promise for addressing senescence in both hair and skin models.[1,5]
Antioxidants: Oxidative stress and senescence often go hand in hand as oxidative stress is a primary driver of cellular senescence, making antioxidants powerful tools for counteracting this damage. Nutrients and compounds that reduce oxidative stress show potential for reversing senescence and promoting hair growth.[13]

Thanks to these solutions—from senolytics to powerful antioxidants—the era of targeting hair loss at its root is here.

03

The Future of Hair Loss Treatment: Targeting Senescence

Due to the association of senescence and multiple types of hair loss, many experts believe the next generation of hair loss treatments will be focused on combating senescence, the aging process that compromises scalp health and follicle function.[3,4] By targeting senescence in dermal papilla cells (DPCs), outer root sheath cells (ORSCs), and hair follicle stem cells (HFSCs), reducing harmful inflammatory SASP, and combating oxidative stress, these cutting-edge therapies have the potential to address the root causes of follicular aging to restore the vitality of your hair:

Senolytics: Senolytics are a class of molecules that selectively target senescent cells and cause them to undergo apoptosis (programmed cell death), helping minimize their harmful effects on the body. Research shows that senolytic treatments, like quercetin and dasatinib, can mitigate their negative impact on the hair follicle microenvironment, presenting a promising strategy for restoring hair growth and combating hair loss by reducing senescent cells in the hair follicle.[4] Other researchers have found that senolytic treatment could partially reverse age-related hair loss in both normal aged mice, as well as genetically fast-aging mice by restoring tissue homeostasis within the hair follicle and promote hair growth.[3]
Senomorphics: Senomorphic molecules target senescence by reducing the expression of inflammatory factors called SASP from senescent cells, preventing their spread. Researchers suspect that reducing SASP-driven inflammation improves the regenerative environment, supporting the recovery of hair follicle activity and promoting new hair growth.[3] Therapies like rapamycin and metformin have shown promise for their potential to suppress damaging inflammatory factors such as IL-6, which could mitigate hair follicle damage.[13] Additionally, our OS-01 peptide has been shown to act as a senomorphic and shows promise for addressing senescence in both hair and skin models.[1,5]
Antioxidants: Oxidative stress and senescence often go hand in hand as oxidative stress is a primary driver of cellular senescence, making antioxidants powerful tools for counteracting this damage. Nutrients and compounds that reduce oxidative stress show potential for reversing senescence and promoting hair growth.[13]

Thanks to these solutions—from senolytics to powerful antioxidants—the era of targeting hair loss at its root is here.

Key Takeaways:

Senescence is associated with age-related thinning, pattern balding, and stress-related hair loss, making treatments that reduce senescent cells in hair follicles promising treatments for preventing and reversing hair loss
Hair follicles exposed to inflammatory stress from senescent cells atrophy over time, producing thinner and weaker strands.
The dermal papilla cells (DPCs) at the base of hair follicles act as conductors to surrounding cells like outer root sheath cells (ORSCs) which are critical to hair growth, but lose efficiency as they age and accumulate damage.
Androgens and oxidative stress are shown to increase senescence, exacerbating follicular aging and pattern balding.
Unlike pattern balding, age-related thinning isn’t hormone-driven but is thought to stem from the accumulation of senescent cells in follicles.
While not directly caused by cellular senescence, stress-induced hair loss can often cause an increase in senescent cells, which can lead to hair loss.
Emerging treatments like senolytics combat cellular senescence, addressing hair loss at the root.

Key Takeaways:

Senescence is associated with age-related thinning, pattern balding, and stress-related hair loss, making treatments that reduce senescent cells in hair follicles promising treatments for preventing and reversing hair loss
Hair follicles exposed to inflammatory stress from senescent cells atrophy over time, producing thinner and weaker strands.
The dermal papilla cells (DPCs) at the base of hair follicles act as conductors to surrounding cells like outer root sheath cells (ORSCs) which are critical to hair growth, but lose efficiency as they age and accumulate damage.
Androgens and oxidative stress are shown to increase senescence, exacerbating follicular aging and pattern balding.
Unlike pattern balding, age-related thinning isn’t hormone-driven but is thought to stem from the accumulation of senescent cells in follicles.
While not directly caused by cellular senescence, stress-induced hair loss can often cause an increase in senescent cells, which can lead to hair loss.
Emerging treatments like senolytics combat cellular senescence, addressing hair loss at the root.

References

Zonari, A., et al. Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models. npj Aging, 9(1), 1-15. 2023. https://www.nature.com/articles/s41514-023-00109-1
Zonari A., et al. Double-blind, vehicle-controlled clinical investigation of peptide OS-01 for skin rejuvenation. J Cosmet Dermatol. 2024. https://onlinelibrary.wiley.com/doi/full/10.1111/jocd.16242
https://pmc.ncbi.nlm.nih.gov/articles/PMC5556182/
https://pubmed.ncbi.nlm.nih.gov/39614601/
Based on data from clinical studies and/or lab studies conducted on human skin samples, 3D skin models, and skin or hair cells in the OneSkin lab. Explore more at oneskin.co/claims
https://pmc.ncbi.nlm.nih.gov/articles/PMC3621486/
https://www.cell.com/current-biology/fulltext/S0960-9822(05)00747-5
https://pmc.ncbi.nlm.nih.gov/articles/PMC3026732/
https://pmc.ncbi.nlm.nih.gov/articles/PMC8929036/
https://www.sciencedirect.com/science/article/abs/pii/S0923181117300269
https://www.sciencedirect.com/science/article/pii/S1534580720302318
https://www.sciencedirect.com/science/article/abs/pii/S0378512214003259
https://karger.com/drm/article/239/4/533/836627/Cellular-Senescence-Ageing-and-Androgenetic
https://www.jidonline.org/article/S0022-202X(15)33852-5/fulltext
https://pmc.ncbi.nlm.nih.gov/articles/PMC11068553/
https://pmc.ncbi.nlm.nih.gov/articles/PMC3935391/
https://www.sciencedirect.com/science/article/pii/S0306987717310411
https://pmc.ncbi.nlm.nih.gov/articles/PMC4041217/
https://www.jidonline.org/article/S0022-202X(15)37231-6/fulltext
https://journals.lww.com/ijot/fulltext/2022/14060/hair_aging_and_hair_disorders_in_elderly_patients.1.aspx
https://pmc.ncbi.nlm.nih.gov/articles/PMC6369639/
https://pmc.ncbi.nlm.nih.gov/articles/PMC7310274/
https://www.pnas.org/doi/10.1073/pnas.1901720117
https://pubmed.ncbi.nlm.nih.gov/23385670/

References

Zonari, A., et al. Senotherapeutic peptide treatment reduces biological age and senescence burden in human skin models. npj Aging, 9(1), 1-15. 2023. https://www.nature.com/articles/s41514-023-00109-1
Zonari A., et al. Double-blind, vehicle-controlled clinical investigation of peptide OS-01 for skin rejuvenation. J Cosmet Dermatol. 2024. https://onlinelibrary.wiley.com/doi/full/10.1111/jocd.16242
https://pmc.ncbi.nlm.nih.gov/articles/PMC5556182/
https://pubmed.ncbi.nlm.nih.gov/39614601/
Based on data from clinical studies and/or lab studies conducted on human skin samples, 3D skin models, and skin or hair cells in the OneSkin lab. Explore more at oneskin.co/claims
https://pmc.ncbi.nlm.nih.gov/articles/PMC3621486/
https://www.cell.com/current-biology/fulltext/S0960-9822(05)00747-5
https://pmc.ncbi.nlm.nih.gov/articles/PMC3026732/
https://pmc.ncbi.nlm.nih.gov/articles/PMC8929036/
https://www.sciencedirect.com/science/article/abs/pii/S0923181117300269
https://www.sciencedirect.com/science/article/pii/S1534580720302318
https://www.sciencedirect.com/science/article/abs/pii/S0378512214003259
https://karger.com/drm/article/239/4/533/836627/Cellular-Senescence-Ageing-and-Androgenetic
https://www.jidonline.org/article/S0022-202X(15)33852-5/fulltext
https://pmc.ncbi.nlm.nih.gov/articles/PMC11068553/
https://pmc.ncbi.nlm.nih.gov/articles/PMC3935391/
https://www.sciencedirect.com/science/article/pii/S0306987717310411
https://pmc.ncbi.nlm.nih.gov/articles/PMC4041217/
https://www.jidonline.org/article/S0022-202X(15)37231-6/fulltext
https://journals.lww.com/ijot/fulltext/2022/14060/hair_aging_and_hair_disorders_in_elderly_patients.1.aspx
https://pmc.ncbi.nlm.nih.gov/articles/PMC6369639/
https://pmc.ncbi.nlm.nih.gov/articles/PMC7310274/
https://www.pnas.org/doi/10.1073/pnas.1901720117
https://pubmed.ncbi.nlm.nih.gov/23385670/

Reviewed by Alessandra Zonari, PhD, Chief Scientific Officer (CSO) and Co-Founder of OneSkin

Alessandra earned her Master’s degree in stem cell biology, and her PhD in skin regeneration and tissue engineering at the Federal University of Minas Gerais in Brazil in collaboration with the 3B’s Research Group in Portugal. Alessandra did a second post-doctoral at the University of Coimbra in Portugal. She is a co-inventor of three patents and has published 20 peer-reviewed papers in scientific journals.

Reviewed by Alessandra Zonari, PhD, Chief Scientific Officer (CSO) and Co-Founder of OneSkin

Alessandra earned her Master’s degree in stem cell biology, and her PhD in skin regeneration and tissue engineering at the Federal University of Minas Gerais in Brazil in collaboration with the 3B’s Research Group in Portugal. Alessandra did a second post-doctoral at the University of Coimbra in Portugal. She is a co-inventor of three patents and has published 20 peer-reviewed papers in scientific journals.

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