scholarly journals Brain metabolism in Alzheimer's dementia: studies of 11C-deoxyglucose accumulation, CSF monoamine metabolites and neuropsychological test performance in patients and healthy subjects.

1991 ◽  
Vol 54 (8) ◽  
pp. 672-678 ◽  
Author(s):  
H Nyback ◽  
H Nyman ◽  
G Blomqvist ◽  
I Sjogren ◽  
S Stone-Elander
1989 ◽  
Vol 14 (1-2) ◽  
pp. 89-95 ◽  
Author(s):  
J. Jolkkonen ◽  
E.-L. Helkala ◽  
R. Kutvonen ◽  
M. Lehtinen ◽  
P.J. Riekkinen

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Simon Chiu ◽  
Nigel Gericke ◽  
Michel Farina-Woodbury ◽  
Vladimir Badmaev ◽  
Hana Raheb ◽  
...  

Introduction. Converging evidence suggests that PDE-4 (phosphodiesterase subtype 4) plays a crucial role in regulating cognition via the PDE-4-cAMP cascade signaling involving phosphorylated cAMP response element binding protein (CREB).Objective. The primary endpoint was to examine the neurocognitive effects of extractSceletium tortuosum(Zembrin) and to assess the safety and tolerability of Zembrin in cognitively healthy control subjects.Method. We chose the randomized double-blind placebo-controlled cross-over design in our study. We randomized normal healthy subjects (totaln=21) to receive either 25 mg capsule Zembrin or placebo capsule once daily for 3 weeks, in a randomized placebo-controlled 3-week cross-over design. We administered battery of neuropsychological tests: CNS Vital Signs and Hamilton depression rating scale (HAM-D) at baseline and regular intervals and monitored side effects with treatment emergent adverse events scale.Results. 21 subjects (mean age: 54.6 years ± 6.0 yrs; male/female ratio: 9/12) entered the study. Zembrin at 25 mg daily dosage significantly improved cognitive set flexibility (P<0.032) and executive function (P<0.022), compared with the placebo group. Positive changes in mood and sleep were found. Zembrin was well tolerated.Conclusion. The promising cognitive enhancing effects of Zembrin likely implicate the PDE-4-cAMP-CREB cascade, a novel drug target in the potential treatment of early Alzheimer’s dementia. This trial is registered with ClinicalTrials.govNCT01805518.


2019 ◽  
Vol 41 (1) ◽  
pp. 5-16 ◽  
Author(s):  
Evangeline Yee ◽  
Karteek Popuri ◽  
Mirza Faisal Beg ◽  

2021 ◽  
Vol 11 ◽  
Author(s):  
Md. Sahab Uddin ◽  
Md. Motiar Rahman ◽  
Mohammad Abu Sufian ◽  
Philippe Jeandet ◽  
Ghulam Md. Ashraf ◽  
...  

Alzheimer’s disease (AD) is the most common form of dementia, which causes abnormalities in learning, thinking, memory, as well as behavior. Generally, symptoms of AD develop gradually and aggravate over time, and consequently severely interfere with daily activities. Furthermore, obesity is one of the common risk factors for dementia. Dysregulation of adipokine and adipocyte dysfunction are assumed to be accountable for the high risk of obesity in people that develop many related disorders such as AD. Moreover, it has been observed that the dysfunction of adipose is connected with changes in brain metabolism, brain atrophy, cognitive decline, impaired mood, neuroinflammation, impaired insulin signaling, and neuronal dysfunction in people with obesity. Conversely, the pathological mechanisms, as well as the molecular players which are involved in this association, have been unclear until now. In this article, we discuss the impact of adiponectin (AdipoQ) on obesity-related Alzheimer’s dementia.


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