Emerging Evidence Linking Gonadotropins to Cognition, Mood, Neuroendocrine Signaling, and Healthy Brain Aging

Dr. Deanna Minich, PhD, MS, CNS, FMCP, FACN

Chief Science Officer, Symphony Natural Health

Follicle-stimulating hormone (FSH) is no longer understood as a purely reproductive signal: FSH receptors have been identified in the hippocampus and cerebral cortex — brain regions central to memory and learning — and rising FSH during the menopausal transition is increasingly studied as an independent contributor to cognitive risk and mood changes, separate from estrogen decline [1-3].

When conversations turn to menopause and brain health, estrogen usually takes center stage—and for good reason. Declining estrogen has long been linked to changes in memory, mood, and cognitive function [4]. But researchers are beginning to look beyond estrogen alone.

One hormone receiving increasing attention is follicle-stimulating hormone (FSH), which rises early in the menopausal transition and may play a broader physiological role than previously recognized. Traditionally viewed as a reproductive hormone responsible for ovarian follicle development, FSH is now being investigated for potential effects throughout the body—including the brain. While research remains in its early stages, emerging evidence suggests that rising FSH levels may influence healthy neuroinflammatory balance, brain structure, cognitive function, and processes involved in healthy neuronal function.

Menopause and the Changing Neuroendocrine Landscape

One of the earliest hormonal changes in the menopausal transition is a rise in FSH [5]. FSH often begins increasing years before a substantial drop in estrogen. It can rise nearly tenfold after menopause [5,6]. This increase was historically viewed mainly as a marker of ovarian aging. As ovarian function changes, the pituitary gland produces more FSH to try to stimulate follicular activity [7].

At the same time, estrogen has long been recognized as a critical regulator of brain health. Estrogen supports neuronal survival, cerebral glucose metabolism, mitochondrial function, synaptic plasticity, and neurovascular integrity, while promoting the growth and maintenance of dendritic spines, the specialized structures on neurons that facilitate communication between brain cells [8-11]. Experimental studies have shown that fluctuations and eventual declines in estrogen are associated with reduced dendritic spine density, particularly within the hippocampus and prefrontal cortex, brain regions essential for learning, memory, and executive function [12,13]. These established neuroprotective actions of estrogen have historically shaped the view that neurological changes during menopause are driven primarily by estrogen deficiency.

Rather than replacing estrogen as the principal neuroendocrine regulator, emerging evidence suggests that rising FSH may represent an additional endocrine signal that contributes to the remodeling of the menopausal brain. This has led researchers to reconsider whether FSH is simply a marker of ovarian aging or whether it may also contribute to some of the physiological changes that accompany menopause.

This concept first gained attention nearly two decades ago when researchers reviewing findings from the Women's Health Initiative Memory Study proposed that elevated gonadotropins—including FSH—might contribute to age-related neurological changes beyond the effects of estrogen loss alone [14,15]. While these early hypotheses were largely theoretical, they helped spark a new area of investigation that continues today.

"For decades we've viewed menopause through the lens of estrogen decline. However, researchers like Dr. Lisa Mosconi have begun to change that conversation. While estrogen remains fundamental to brain health, emerging science suggests we may be overlooking another important endocrine messenger. FSH may help us better understand when the brain begins adapting to midlife and why cognitive experiences vary so much from one woman to another." - Dr. Deanna Minich, PhD, MS, CNS, FMCP, FACN

FSH and Cognition: What the Research Suggests

Historically, FSH was named for its role in stimulating ovarian follicles [9,10]. That designation made sense when reproductive biology was the primary focus of investigation.

However, accumulating evidence suggests that FSH may be involved in physiological processes beyond the ovary. Studies have linked FSH signaling to bone remodeling [11], energy metabolism [12,13], body composition [3], lipid regulation and vascular health [14], neuroendocrine function [15-17], and potentially immune and stem cell regulation [18]. The identification of FSH receptors in multiple non-reproductive tissues supports the possibility that FSH is more accurately conceptualized as a pituitary-derived synchronizing signal that reflects the whole-body endocrine state.

This does not mean that FSH directly causes aging. Rather, it suggests that FSH may reflect and potentially participate in the broader endocrine adaptations and in some respects decline occurring during midlife and beyond

The Bigger Story: FSH Is Part of an Endocrine Network

FSH Receptors are Found in the Brain.

One reason interest in FSH has expanded is the discovery of FSH receptors (FSHRs) outside the reproductive system.

Recent animal studies have identified FSHRs in several brain regions involved in learning, memory, and cognitive processing, including the hippocampus and cerebral cortex [1-3].

The presence of these receptors suggests that FSH may be capable of acting directly within the central nervous system rather than influencing brain function only through changes in estrogen production.

Experimental studies further suggest that FSH signaling may affect pathways involved in:

• Brain lipid regulation [2,16]
• Cellular energy metabolism [2]
• Neuroinflammatory balance [17]
• Neurotransmitter signaling [17]
• Synaptic plasticity [17]

Many of these same pathways are increasingly recognized as important contributors to age-related changes in cognition and neuronal function. In animal models, FSH signaling has been linked to pathways involved in amyloid-beta and tau accumulation, two hallmark features of Alzheimer's disease. Whether the same mechanisms operate in humans remains an active area of investigation [1].

FSH and Cognitive Function

Human studies examining FSH and cognition are still relatively limited, but several findings have generated considerable interest.

Large observational studies have reported that higher FSH concentrations are associated with poorer cognitive performance and may represent a risk factor for age-related cognitive changes in postmenopausal women [3,18].

Additional research has linked higher FSH levels with increased white matter hyperintensity volume—a marker of small-vessel changes within the brain that have been associated with cognitive risk [19].

Importantly, many of these associations persist even after accounting for traditional cardiovascular risk factors, suggesting that FSH may capture unique aspects of the menopausal transition.

FSH May Influence Cognitive Health Independent of Estrogen

World-renowned neuroscientist Lisa Mosconi, PhD, whose research focuses on Alzheimer's disease (AD), women's brain health, and neuroimaging, has described menopause as a "neuroendocrine transition state," emphasizing that the menopausal transition reflects coordinated changes across the brain and endocrine system [20].

Consistent with this perspective, her research team identified FSH as a potential biomarker of brain aging in midlife women [21]. In a 2023 clinical study of 191 women aged 40–65 years at risk for late-onset AD, higher serum FSH concentrations were associated with greater cerebral amyloid-β (Aβ) burden and reduced gray matter volume in Alzheimer's disease–vulnerable brain regions, suggesting that FSH may serve as an early endocrine indicator of neurodegenerative risk during the menopausal transition [21].

Effects were most pronounced in postmenopausal women, with effects detectable as early as perimenopause. These associations remained significant after adjusting for:

• Age
• APOE-4 status
• Estradiol levels
• Hormone therapy use
• Other clinical variables

Interestingly, women with higher FSH did not perform differently on cognitive testing despite these imaging findings [21]. This raises the possibility that structural brain changes, if they are occurring, may precede noticeable symptoms. Interestingly, no significant differences in cognitive testing were observed despite measurable structural brain changes. This raises the possibility that FSH-associated alterations may occur years before symptoms become clinically apparent.

At the same time, findings remain inconsistent across studies. Researchers believe this variability likely reflects the complex interactions among FSH, estrogen, sleep quality, vasomotor symptoms, metabolic health, vascular function, and aging itself [22,23]. For this reason, FSH should currently be viewed as a potential biomarker of brain aging rather than a confirmed causal driver of cognitive aging. Human intervention studies targeting FSH have not yet established whether modifying FSH levels influences age-related cognitive changes.

A Side Note About FSH in Men and Alzheimer’s Disease

Although most research on FSH and brain health has focused on women because of the marked rise in FSH during menopause, recent studies suggest that its effects may extend to men as well. In a cross-sectional study of adults over 80 years of age, higher FSH concentrations were associated with a greater likelihood of Alzheimer's disease-related dementia, particularly in men, even after accounting for LH and other clinical factors [23]. Estradiol and testosterone concentrations did not differ between cognitive groups, suggesting that the relationship was not simply explained by differences in circulating sex steroids.

More recently, a longitudinal analysis of 490 adults with mild cognitive impairment or Alzheimer's disease from the ADNI cohort found that higher baseline FSH predicted faster cognitive decline and greater temporal lobe atrophy over time, independent of age, sex, APOE ε4 status, and other clinical variables [24]. Together, these studies suggest that elevated FSH may be associated not only with biomarkers of brain aging in women, but also with disease progression across both sexes.

Genetics May Matter

Researchers are also beginning to investigate whether FSH interacts with genetic risk factors for age-related cognitive changes.

One of the most important is the APOE4 genotype, which influences cognitive risk in women. Experimental evidence suggests that APOE4 and FSH may work together to activate signaling pathways involved in neuronal health [25]. Consistent with these findings, another study found that both APOE4 status and FSH levels independently predicted amyloidogenic processes associated with age-related cognitive changes in postmenopausal women, whereas estradiol did not [18].

These observations raise the possibility that certain women may be more vulnerable to the neurological effects of rising FSH during aging.

"The brain doesn't age in isolation. It is part of the HPTAO axis and in constant conversation with the gastrointestinal, immune, metabolic, and musculoskeletal systems. That's why supporting cognitive health during menopause requires more than replacing a single hormone. It calls for strengthening the resilience of the entire neuroendocrine network through nutrition, movement, sleep, circadian health, stress management, and targeted nutritional support."     - Dr. Deanna Minich, PhD, MS, CNS, FMCP, FACN

FSH, Stress Resilience, and Mood

One of the most intriguing areas of research involves neuroinflammatory balance within the brain.

In animal models, exposure to elevated FSH levels increased the production of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β), while also altering synaptic plasticity and producing behaviors associated with low mood [17]. Researchers also observed alterations in glutamate and gamma-aminobutyric acid (GABA) signaling—two neurotransmitter systems involved in mood regulation, stress resilience, and cognitive performance [17].

Though not causal, these findings suggest that rising FSH levels may interact with neuroinflammatory pathways that influence emotional well-being during the menopausal transition.

Given that mood changes commonly emerge during perimenopause, this remains an important area for future research.

A Broader View: The Brain Doesn't Function in Isolation

The brain doesn't function in isolation. It constantly communicates with bone, adipose tissue, skeletal muscle, and other metabolically active organs through hormones, cytokines, and other signaling molecules. Because FSH appears to influence several of these tissues, some of its effects on brain health may be indirect rather than occurring entirely within the brain itself.

Emerging research suggests that FSH participates in a broader endocrine network involving:

• Adipose tissue [6]
• Bone [26]
• Inflammatory signaling [17]
• Lipid regulation [27]
• Skeletal muscle [28]

These systems continuously communicate with the brain through hormones, cytokines, adipokines, and other signaling molecules [29,30]. As a result, FSH-related changes in body composition, metabolic health, and inflammatory signaling may influence cognitive aging even if direct effects within the brain are modest.

While many questions remain, this research reinforces a broader point: menopause involves far more than declining estrogen. As researchers continue to untangle the roles of different hormones, FSH is emerging as another piece of the puzzle. Whether it ultimately proves to be a driver of age-related brain changes, a marker of those changes, or both remains to be determined, but it highlights the importance of viewing menopause through a broader neuroendocrine lens.

Strategies to Support Cognitive Health in Midlife

Encourage Physical Activity. Exercise supports several factors associated with cognition, including cardiovascular health, cerebral circulation, and healthy levels of brain-derived neurotrophic factor (BDNF), which supports memory, synaptic plasticity, and neuronal health [31]. Both aerobic and strength training can support cognitive health in midlife women [32].

Support Restful Sleep. Healthy sleep supports normal clearance of metabolic waste within the brain, maintenance of neurotransmitter levels, and hormone balance [33].

Maintain Healthy Eating Habits. Dietary patterns, such as the MIND diet, may support cognitive function and brain health [34]. The MIND diet combines elements of the Mediterranean and DASH diets. It encourages consumption of plant-based, antioxidant-rich foods such as whole grains, leafy greens and other vegetables, berries, nuts, beans, and olive oil, as well as fish and lean meats.

Address Endocrine Function with Targeted Supplements. The standardized, concentrated, bioavailable, clinically tested formulation of Lepidium peruvianum (maca), known as FemmenessencePRO™, has been shown to support healthy function of the hypothalamic-pituitary-thyroid-adrenal-ovarian (HPTAO) axis, with favorable effects on endocrine biomarkers, including FSH and estradiol, alongside improvements in menopausal symptoms [35-37]. By supporting this interconnected endocrine network, FemmenessencePRO™ may also help promote healthy brain aging, cognitive function, and neuroendocrine adaptation during the menopausal transition.

Monitor the Status of Key Nutrients. Certain nutrients, like vitamin B12 and folic acid, can influence cognitive function [38]. Additionally, iron dynamics shift in menopause, and maintaining healthy levels can support cognitive function [39].

Consider Health History. Some mental health concerns or alterations in thyroid hormone metabolism can exacerbate cognitive changes in menopause and may warrant attention [38].

Manage Chronic Stress. Supporting healthy stress resilience through adequate sleep, mindfulness practices, time outdoors, physical activity, or other stress-management techniques may help support overall brain and cognitive health [40,41].

Educate About Endocrine Disruptors. Emerging research suggests that endocrine disrupting chemicals (EDCs) may alter FSH-FSHR signaling and contribute to premature ovarian insufficiency [42,43]. Additionally, EDC exposure is associated with altered cognitive function [44].

Dr. Deanna Minich, PhD, MS, CNS, FMCP, FACN

Chief Science Officer, Symphony Natural Health

Nutrition scientist, researcher, educator, and author with 25+ years across academia and the supplement industry, including most recently as a featured expert in nutrition and functional medicine in the PBS documentary The (M) Factor 2.

PhD in Medical Sciences; MS in Human Nutrition and Dietetics; Certified Nutrition Specialist. Recipient of the 2025 Linus and Ava Helen Pauling Award, the highest honor in Functional Medicine, with past winners including Dr. Mark Hyman, Dr. Dean Ornish, and Dr. Terry Wahls.

She spent ten years working with Dr. Jeffrey Bland on the research and development team at Metagenics, engaged in global strategy and education related to functional medicine and natural products, and helped establish his Personalized Lifestyle Medicine Institute (PLMI) in 2014. She is currently on the Board of Directors for PLMI. Past President, American College of Nutrition; fellow of the American College of Nutrition (FACN); Board of Directors for 7 years, American Nutrition Association; Nutrition Advisory Board, Institute for Functional Medicine; and has been an educator for the Institute for Functional Medicine and University of Western States for over a decade.

Author of seven consumer books including the Rainbow Diet, and 50+ scientific publications. Oversees and guides Symphony's Medical and Science Team focusing on researching the root cause of women's health and hormone imbalance conditions. She is the lead author on the most recent FSH paper and is dedicated to empowering women to understand their whole health and supporting endocrine health throughout life. Has trained thousands of healthcare professionals and educated consumers worldwide over the past 25 years through her presentations and courses.

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