Can Genetic Markers Predict the Sporadic Form of Alzheimer’s Disease? An Updated Review on Genetic Peripheral Markers

Theron, Danelda; Hopkins, Lloyd N.; Sutherland, Heidi G.; Griffiths, Lyn R.; Fernandez, Francesca

doi:10.3390/ijms241713480

Cited by 2 publications

(1 citation statement)

References 159 publications

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“…It accounts for 50% to 75% of diagnosed dementia cases [ 3 ]. AD is classified into two types: senile (sporadic), which is predominant in 95–98% of cases, and presenile (familial) [ 4 , 5 ]. It is hypothesized that the neurodegenerative processes associated with sporadic AD may begin as early as 20 years before the onset of clinical symptoms [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

Unlocking the Potential: Semaglutide’s Impact on Alzheimer’s and Parkinson’s Disease in Animal Models

Meca,

Boboc,

Mititelu-Tartau

et al. 2024

CIMB

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Semaglutide (SEM), a glucagon-like peptide-1 receptor agonist, has garnered increasing interest for its potential therapeutic effects in neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). This review provides a comprehensive description of SEM’s mechanism of action and its effects in preclinical studies of these debilitating conditions. In animal models of AD, SEM has proved beneficial effects on multiple pathological hallmarks of the disease. SEM administration has been associated with reductions in amyloid-beta plaque deposition and mitigation of neuroinflammation. Moreover, SEM treatment has been shown to ameliorate behavioral deficits related to anxiety and social interaction. SEM-treated animals exhibit improvements in spatial learning and memory retention tasks, as evidenced by enhanced performance in maze navigation tests and novel object recognition assays. Similarly, in animal models of PD, SEM has demonstrated promising neuroprotective effects through various mechanisms. These include modulation of neuroinflammation, enhancement of mitochondrial function, and promotion of neurogenesis. Additionally, SEM has been shown to improve motor function and ameliorate dopaminergic neuronal loss, offering the potential for disease-modifying treatment strategies. Overall, the accumulating evidence from preclinical studies suggests that SEM holds promise as a novel therapeutic approach for AD and PD. Further research is warranted to elucidate the underlying mechanisms of SEM’s neuroprotective effects and to translate these findings into clinical applications for the treatment of these devastating neurodegenerative disorders.

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