Primary Hypothyroidism and Alzheimer’s Disease: A Tale of Two

Alanazi, Faisal; Al-Kuraishy, Hayder M; Αλεξίου, Αθανάσιος; Papadakis, Marios; Ashour, Mahmoud; Alnaaim, Saud; Elhussieny, Omnya; Saad, Hebatallah M.; Batiha, Gaber El‐Saber

doi:10.1007/s10571-023-01392-y

Cited by 16 publications

(7 citation statements)

References 115 publications

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“…Besides, oxidative stress and inflammation in different systemic diseases may reduce the function of the thyroid gland leading to PHT [ 38 ]. Interestingly, long-term PHT can affect the functions of the CNS and increase the risk for the development of Alzheimer's disease (AD) by triggering inflammation and oxidative stress which play a critical role in the pathogenesis of AD [ 39 ].…”

Section: Primary Hypothyroidismmentioning

confidence: 99%

Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism

Alomair,

Al-Kuraishy,

Al-Gareeb

et al. 2024

Thyroid Res

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Primary hypothyroidism (PHT) is associated with an increased risk for the development of atherosclerosis (AS) and other cardiovascular disorders. PHT induces atherosclerosis (AS) through the induction of endothelial dysfunction, and insulin resistance (IR). PHT promotes vasoconstriction and the development of hypertension. However, patients with subclinical PHT with normal thyroid hormones (THs) are also at risk for cardiovascular complications. In subclinical PHT, increasing thyroid stimulating hormone (TSH) levels could be one of the causative factors intricate in the progression of cardiovascular complications including AS. Nevertheless, the mechanistic role of PHT in AS has not been fully clarified in relation to increased TSH. Therefore, in this review, we discuss the association between increased TSH and AS, and how increased TSH may be involved in the pathogenesis of AS. In addition, we also discuss how L-thyroxine treatment affects the development of AS.

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Section: Primary Hypothyroidismmentioning

confidence: 99%

Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism

Alomair,

Al-Kuraishy,

Al-Gareeb

et al. 2024

Thyroid Res

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“…AD neuropathology is developed due to extracellular accumulation of neurotoxic amyloid beta (Aβ) and intracellular deposition of hyperphosphorylated tau protein which form neurofibrillary tangles (NFTs). 53 , 54 It has been shown that the over‐activation of brain RAS is associated with the development of cognitive impairment and memory deficits. 55 It has been illustrated that overactivity of RAS in hypertensive patients triggers the development and progression of AD by activating of neuronal AT1R which induce oxidative stress and neuroinflammation.…”

Section: Role Of Brain Ras In Neurodegenerative Di...mentioning

confidence: 99%

“…AD is the commonest neurodegenerative disease in elderly and represents two third of all dementia cases. AD neuropathology is developed due to extracellular accumulation of neurotoxic amyloid beta (Aβ) and intracellular deposition of hyperphosphorylated tau protein which form neurofibrillary tangles (NFTs) 53,54 . It has been shown that the over‐activation of brain RAS is associated with the development of cognitive impairment and memory deficits 55 .…”

Section: Role Of Brain Ras In Neurodegenerative Diseasesmentioning

confidence: 99%

The potential role of brain renin‐angiotensin system in the neuropathology of Parkinson disease: Friend, foe or turncoat?

Al‐Qahtani,

Al‐kuraishy,

Al‐Gareeb

et al. 2024

J Cellular Molecular Medi

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Parkinson disease (PD) is one of the most common neurodegenerative diseases of the brain. Of note, brain renin‐angiotensin system (RAS) is intricate in the PD neuropathology through modulation of oxidative stress, mitochondrial dysfunction and neuroinflammation. Therefore, modulation of brain RAS by angiotensin receptor blockers (ARBs) and angiotensin‐converting enzyme inhibitors (ACEIs) may be effective in reducing the risk and PD neuropathology. It has been shown that all components including the peptides and enzymes of the RAS are present in the different brain areas. Brain RAS plays a critical role in the regulation of memory and cognitive function, and in the controlling of central blood pressure. However, exaggerated brain RAS is implicated in the pathogenesis of different neurodegenerative diseases including PD. Two well‐known pathways of brain RAS are recognized including; the classical pathway which is mainly mediated by AngII/AT1R has detrimental effects. Conversely, the non‐classical pathway which is mostly mediated by ACE2/Ang1‐7/MASR and AngII/AT2R has beneficial effects against PD neuropathology. Exaggerated brain RAS affects the viability of dopaminergic neurons. However, the fundamental mechanism of brain RAS in PD neuropathology was not fully elucidated. Consequently, the purpose of this review is to disclose the mechanistic role of RAS in in the pathogenesis of PD. In addition, we try to revise how the ACEIs and ARBs can be developed for therapeutics in PD.

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“…Analysis of brain tissues of AD patients in a postmortem study revealed that the expression of thyroid hormone receptors was higher than controls [87]. Bavarsad et al [87] suggested that thyroid disorders, either hyperthyroidism or hypothyroidism, may be involved in the pathogenesis of AD as thyroid hormones affect memory and cognitive functions [88,89]. A prospective cross-sectional study of 69 patients showed that thyroid-stimulating hormone levels and thyroid hormones correlated with cerebral tau burden and cognitive dysfunction [88].…”

Section: Neuroserpin In Admentioning

confidence: 99%

The probable role of tissue plasminogen activator/neuroserpin axis in Alzheimer’s disease: a new perspective

Ali,

Al-kuraishy,

Al-Gareeb

et al. 2023

Acta Neurol Belg

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Alzheimer’s disease (AD) is the most common type of dementia associated with amyloid beta (Aβ) deposition. Dysfunction of the neuronal clearance pathway promotes the accumulation of Aβ. The plasminogen-activating system (PAS) is controlled by various enzymes like tissue plasminogen activators (tPA). Neuronal tPA enhances the conversion of plasminogen to plasmin, which cleaves Aβ; this function is controlled by many inhibitors of PAS, including a plasminogen-activating inhibitor (PAI-1) and neuroserpin. Therefore, the objective of the present narrative review was to explore the potential role of tPA/neuroserpin in the pathogenesis of AD. PAI-1 activity is increased in AD, which is involved in accumulating Aβ. Progressive increase of Aβ level during AD neuropathology is correlated with the over-production of PAI-1 with subsequent reduction of plasmin and tPA activities. Reducing plasmin and tPA activities promote Aβ by reducing Aβ clearance. Neuroserpin plays a critical role in the pathogenesis of AD as it regulates the expression and accumulation of Aβ. Higher expression of neuroserpin inhibits the neuroprotective tPA and the generation of plasmin with subsequent reduction in the clearance of Aβ. These observations raise conflicting evidence on whether neuroserpin is neuroprotective or involved in AD progression. Thus, neuroserpin over-expression with subsequent reduction of tPA may propagate AD neuropathology. Graphical abstract

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Primary Hypothyroidism and Alzheimer’s Disease: A Tale of Two

Cited by 16 publications

References 115 publications

Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism

Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism

The potential role of brain renin‐angiotensin system in the neuropathology of Parkinson disease: Friend, foe or turncoat?

The probable role of tissue plasminogen activator/neuroserpin axis in Alzheimer’s disease: a new perspective

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