The impact of luteinizing hormone and testosterone on beta amyloid (Aβ) accumulation: Animal and human clinical studies

Verdile, Giuseppe; Asih, Prita R.; Barron, Anna M.; Wahjoepramono, Eka Julianta; Ittner, Lars M.; Martins, Ralph N.

doi:10.1016/j.yhbeh.2015.05.020

Cited by 28 publications

(37 citation statements)

References 135 publications

(148 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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“…Even elderly men who are above 65 years old with late onset hypogonadism benefit as much as the younger men in terms of safety profile and increasing testosterone levels [4]. With respect to cognition, although cell culture and animal studies have provided support for testosterone in having potential therapeutic benefits in AD [5]. there have been relatively few studies that have trialed testosterone supplementation in men with AD or mild cognitive impairments (MCI) and none have evaluated testosterone treatment in individuals that are pre-symptomatic but at a greater risk of cognitive decline.…”

Section: Introductionmentioning

confidence: 99%

The Effects of Testosterone Supplementation on Cognitive Functioning in Older Men.

Wahjoepramono¹,

Asih²,

Aniwiyanti³

et al. 2016

CNSNDDT

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Reduction in testosterone levels in men during aging is associated with cognitive decline and risk of dementia. Animal studies have shown benefits for testosterone supplementation in improving cognition and reducing Alzheimer’s disease pathology. In a randomized, placebo-controlled, crossover study of men with subjective memory complaint and low testosterone levels, we investigated whether testosterone treatment significantly improved performance on various measures of cognitive functioning. Forty-four men were administered a battery of neuropsychological tests to establish the baseline prior to being randomly divided into two groups. The first group (Group A) received 24 weeks of testosterone treatment (T treatment) followed by 4 weeks washout, and then 24 weeks of placebo (P); the second group (Group B) received the same treatments, in reverse order (Placebo, washout, and then T treatment). In group A (TèP), compared to baseline, there was a modest (1 point) but significant improvement in general cognitive functioning as measured by the Mini Mental State Examination (MMSE) following testosterone treatment. This improvement from baseline was sustained following the washout period and crossover to placebo treatment. Similar Mini Mental State Examination (MMSE) scores were observed when comparing testosterone treatment with placebo. In group B (PèT) a significant increase was observed from baseline following testosterone treatment and a trend towards an increase when compared to placebo treatment. Improvements in baseline depression scores (assessed by Geriatric Depression Scale) were observed following testosterone/placebo treatment in both groups, and no difference was observed when comparing testosterone with placebo treatment. Our findings indicate a modest improvement on global cognition with testosterone treatment. Larger clinical trials with a longer follow- up and with the inclusion of blood and brain imaging markers are now needed to conclusively determine the significance of testosterone treatment.

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“…Hormonal processes underlying LOAD are gaining renewed interest [12,13], as GnRH function in the brain has been recently linked to aging [14]. A recent study has shown that increasing levels in plasma of luteinizing hormone, whose secretion is regulated by GnRH, increment brain amyloid burden, which depended on the presence of APOE-E4, for example, rs429358 [15].…”

Section: Discussionmentioning

confidence: 99%

APOE and MS4A6A interact with GnRH signaling in Alzheimer's disease: Enrichment of epistatic effects

Cáceres

Vargas

González

2016

Alzheimer's & Dementia

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The impact of luteinizing hormone and testosterone on beta amyloid (Aβ) accumulation: Animal and human clinical studies

Cited by 28 publications

References 135 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

The Effects of Testosterone Supplementation on Cognitive Functioning in Older Men.

APOE and MS4A6A interact with GnRH signaling in Alzheimer's disease: Enrichment of epistatic effects

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