Luteinizing hormone as a key player in the cognitive decline of Alzheimer's disease

Burnham, Veronica L.; Thornton, Janice E.

doi:10.1016/j.yhbeh.2015.05.010

Cited by 27 publications

(17 citation statements)

References 172 publications

(198 reference statements)

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“…Similarly, increased serum LH concentrations are negatively correlated with cognition in postmenopausal women but positively correlated with serum FSH [58]. In conjugation with estrogen, elevated levels of LH are also associated with an increased risk of developing AD and have a role in the metabolism and accumulation of Aβ [59, 60]. During the onset of the menopause, there is a substantial decrease in estrogen and a significant increase in LH levels with the incidence of AD [61].…”

Section: Endocrinal Dysregulations In the Ad Pathophysiologymentioning

confidence: 99%

Role of Hypothalamic-Pituitary-Adrenal Axis, Hypothalamic-Pituitary-Gonadal Axis and Insulin Signaling in the Pathophysiology of Alzheimer’s Disease

Ahmad

Fatima

Mondal³

2019

Neuropsychobiology

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Alzheimer’s disease (AD), the commonest progressive neurodegenerative disorder of the brain, is clinically characterized by the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles. Recent studies suggest a relationship between the endocrinal dysregulation and the neuronal loss during the AD pathology. Dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis and hypothalamic-pituitary-gonadal (HPG) axis regulating circulating levels of glucocorticoid hormones has been implicated in the pathophysiology of AD. Likewise, dysregulated insulin signaling, impaired glucose uptake and insulin resistance are some of the prime factors in the onset/progression of AD. In this review, we have discussed the changes in HPA and HPG axes, implicated insulin resistance/signaling and glucose regulation during the onset/progression of AD. Therefore, simultaneous detection of these endocrinal markers in the early or presymptomatic stages may help in the early diagnosis of AD. This evidence for implicated endocrinal functions supports the fact that modulation of endocrinal pathways can be used as therapeutic targets for AD. Future studies need to determine how the induction or inhibition of endocrinal targets could be used for predictable neuroprotection in AD therapies.

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Section: Endocrinal Dysregulations In the Ad Pathophysiologymentioning

confidence: 99%

Role of Hypothalamic-Pituitary-Adrenal Axis, Hypothalamic-Pituitary-Gonadal Axis and Insulin Signaling in the Pathophysiology of Alzheimer’s Disease

Ahmad

Fatima

Mondal³

2019

Neuropsychobiology

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“… 38 , 39 Moreover, epidemiological and in vivo studies have suggested that LH contributes to cognitive decline and β-amyloid accumulation, which is a pathological AD hallmark. 40 , 41 We did not identify a clinically meaningful hazard on GnRH agonist treatment compared with patients who did not receive ADT. GnRH agonist usage reduces testosterone and LH levels.…”

Section: Discussionmentioning

confidence: 85%

Type of Androgen Deprivation Therapy and Risk of Dementia Among Patients With Prostate Cancer in Taiwan

et al. 2020

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Key Points Question Does the risk of dementia vary by type of androgen deprivation therapy among patients with prostate cancer? Findings In this cohort study of 23 651 patients with newly diagnosed prostate cancer between 2008 and 2015, there was no association of the use of gonadotropin-releasing hormone agonists or orchiectomy with increased dementia risk, while antiandrogen monotherapy use was associated with a 34% increased dementia risk compared with patients who did not receive androgen deprivation therapy. Meaning These findings suggest that the use of antiandrogen monotherapy, but not gonadotropin-releasing hormone agonist or orchiectomy, requires more attention with respect to subsequent risk of dementia.

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“…These androgenic anti-amyloid actions are exerted in both sexes [92,93]. Androgens can also indirectly reduce Aβ accumulation either through enhancing the estrogen pathway or through hypothalamo-hypophyseal-gonadal axis where they inhibit the release of gonadotropin luteinizing hormone secretion by the negative feedback, and it is well known that the latter hormone increases Aβ production by enhancement of APP/β-secretase initiated amyloidogenic pathway [94]. …”

Section: Androgens and Alzheimer's Diseasementioning

confidence: 99%

“…Based on the abundant data supporting the numerous neuroprotective actions of sex hormones in ameliorating many pathological processes occurring in AD, hormonal replacement therapy (HRT) seems to be theoretically beneficial but the translation of this hypothesis to practice met a lot of difficulties which made the use of HRT in AD management still a matter of skepticism [36,94]. The values of female estrogens and progesterone replacement therapies carry controversial results, which are mainly dependent on the timing, dose and duration of their application to the AD predisposed individual.…”

Section: Sex Hormone Therapy Trials For Alzheimer's Diseasementioning

confidence: 99%

Sex Hormones and Alzheimer’s Disease

Bahnasy¹,

El-Heneedy²,

El-Seidy³

2018

Sex Hormones in Neurodegenerative Processes and Diseases

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Alzheimer's disease (AD) is the most common type of dementia and the most common neurodegenerative disorder of elderly. It is not an accelerated form of aging but it is characterized by distinct temporospatial brain pathological changes, including amyloid plaques accumulation, neurofibrillary tangles deposition, synaptic loss and neuronal death with gross brain atrophy. These changes result in persistent progressive memory and cognitive decline interfering with the usual daily activities. AD is a multifactorial disorder results from the interaction of genetic, epigenetic, environmental and lifestyle factors. Estrogen, progesterone and androgen effects are important building stones in AD pathogenesis, and their effect in brain modulation and development results in different gender susceptibility to the disease. These sex hormones whether gonadal or neurosteroids (synthesized locally in the brain) play important neuroprotective roles influencing the individual's vulnerability to AD development, rate of mild cognitive impairment (MCI)/AD conversion and speed of AD progression. Despite the little therapeutic implications of hormonal replacement therapy in AD treatment, yet this topic still represents a challenging hopeful way to construct a strategy for the development of personalized, gender-specific AD management.

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Luteinizing hormone as a key player in the cognitive decline of Alzheimer's disease

Cited by 27 publications

References 172 publications

Role of Hypothalamic-Pituitary-Adrenal Axis, Hypothalamic-Pituitary-Gonadal Axis and Insulin Signaling in the Pathophysiology of Alzheimer’s Disease

Role of Hypothalamic-Pituitary-Adrenal Axis, Hypothalamic-Pituitary-Gonadal Axis and Insulin Signaling in the Pathophysiology of Alzheimer’s Disease

Type of Androgen Deprivation Therapy and Risk of Dementia Among Patients With Prostate Cancer in Taiwan

Sex Hormones and Alzheimer’s Disease

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