Cognitive Impairment in Parkinson’s Disease: Epidemiology, Clinical Profile, Protective and Risk Factors

Gonzàlez‐Latapi, Paulina; Bayram, Ece; Litvan, Irene; Marras, Connie

doi:10.3390/bs11050074

Cited by 58 publications

(26 citation statements)

References 182 publications

(213 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Of note, the study reported that 80% of PD patients were complicated with cognitive impairment, and 30% of patients developed Parkinson's dementia. Some studies have found that the occurrence of dementia in patients with PD is not only related to cognitive impairment but also related to serum inflammatory factors [ 30 ]. Serum MIF is a marker of slow and acute inflammation, which can promote the development of PD.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pramipexole Combined with Nerve Growth Factor on Cognitive Impairment and Urinary AD7c-NTP Expression in Patients with Parkinson’s Disease

Wang

Cheng

2022

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

Objective. To explore the effects of pramipexole combined with nerve growth factor (NGF) on cognitive impairment and urinary Alzheimer-associated neural thread protein (AD7c-NTP) expression in patients with Parkinson’s disease (PD). Methods. Fifty patients with PD treated in our hospital from February 2020 to April 2021 were enrolled. The patients were arbitrarily assigned into control group and study group. The former was treated with pramipexole, and the latter was treated with pramipexole combined with NGF. The efficacy, cognitive function, serum inflammatory factors, cortisol levels, serum macrophage migration inhibitory factor (MIF), brain-derived neurotrophic factor (BDNF), urine AD7c-NTP levels, and the incidence of adverse reactions were compared. Results. First of all, the effective rate in the study group was higher compared to the control group ( P < 0.05 ). After treatment, the cognitive function was enhanced, and the scores of Montreal cognitive assessment (MoCA) in the study group were higher compared to the control group ( P < 0.05 ). The levels of serum IL-6, CRP, and TNF-α decreased after treatment, and the levels of serum IL-6, CRP, and TNF-α in the study group were remarkably lower compared to the control group ( P < 0.05 ). In addition, the levels of serum DA, NE, and 5-HT increased after treatment, and the levels of serum DA, NE, and 5-HT in the study group were remarkably higher compared to the control group ( P < 0.05 ). Then, the levels of serum MIF and urine AD7c-NTP decreased and BDNF increased after treatment, and the level of BDNF in the study group was higher compared to the control group, while the levels of serum MIF and urine AD7c-NTP in the study group were lower compared to the control group ( P < 0.05 ). Finally, the adverse reactions were compared. The incidence of adverse reactions in the study group was lower compared to the control group, and the difference exhibited not statistically significant (16.00% vs. 24.00%, P > 0.05 ). Conclusion.Pramipexole combined with NGF therapy not only can effectively strengthen the cognitive impairment of patients with PD and promote clinical efficacy and high safety but also can inhibit inflammatory state, regulate brain neurotransmitters, and reduce urinary AD7c-NTP levels.

show abstract

Section: Discussionmentioning

confidence: 99%

Effects of Pramipexole Combined with Nerve Growth Factor on Cognitive Impairment and Urinary AD7c-NTP Expression in Patients with Parkinson’s Disease

Wang

Cheng

2022

Computational and Mathematical Methods in Medicine

View full text Add to dashboard Cite

show abstract

“…However, there has been little systematic effort to determine whether Pink1-/-rats also model PD-relevant cognitive or memory phenotypes. This is despite evidence that among genetically determined forms of PD, patients with Pink1 mutations have the greatest incidence of cognitive dysfunction and decline (Piredda, Desmarais et al 2020, Gonzalez-Latapi, Bayram et al 2021). To fill this gap in knowledge, longitudinal testing using Novel Object Recognition (NOR), Novel Object Location (NOL) and Object in Place (OiP) paradigms was used to determine whether and when Pink1 -/-rats express deficits similar to the impairments in visual recognition memory and//or visuospatial information processing that commonly occur in PD patients (Owen, Beksinska et al 1993, Higginson, Wheelock et al 2005, Possin, Filoteo et al 2008, Fang, Lv et al 2020.…”

Section: Introductionmentioning

confidence: 99%

Spontaneous object exploration in a recessive gene knockout model of Parkinson’s disease: Development and progression of object recognition memory deficits in male Pink1-/- rats

Pinizzotto

Dreyer

Aje

et al. 2022

Preprint

View full text Add to dashboard Cite

Cognitive impairments appear at or before motor signs in about one third of patients with Parkinson’s disease (PD) and have a cumulative prevalence of roughly 80% overall. These deficits exact an unrelenting toll on patients’ quality and activities of daily life due in part to a lack of available treatments to ameliorate them. This study used three well-validated novel object recognition-based paradigms to explore the suitability of rats with knockout of the PTEN-induced putative kinase1 gene (Pink1) for investigating factors that induce cognitive decline in PD and for testing new ways to mitigate them. Longitudinal testing of rats from three to nine months of age revealed significant impairments in male Pink1-/- rats compared to wild type controls in Novel Object Recognition, Novel Object Location and Object-in-Place tasks. Task-specific differences in the progression of object discrimination/memory deficits across age were also seen. Finally, testing using an elevated plus maze, a tapered balance beam and a grip strength gauge showed that in all cases recognition memory deficits preceded potentially confounding impacts of gene knockout on affect or motor function. Taken together, these findings suggest that knockout of the Pink1 gene negatively impacts the brain circuits and/or neurochemical systems that support performance in object recognition tasks. Further investigations using Pink1-/-rats and object recognition memory tasks should provide new insights into the neural underpinnings of the visual recognition memory and visuospatial information processing deficits that are often seen in PD patients and accelerate the pace of discovery of better ways to treat them.

show abstract

“…Parkinson’s disease is characterized by a gradual loss and degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Its etiology is associated with several risk factors (environmental factors) and family history) [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Alpha-Synuclein: The Spark That Flames Dopaminergic Neurons, In Vitro and In Vivo Evidence

Henriques¹,

Rouvière²,

Giorla³

et al. 2022

IJMS

View full text Add to dashboard Cite

Mitochondria, α-syn fibrils and the endo-lysosomal system are key players in the pathophysiology of Parkinson’s disease. The toxicity of α-syn is amplified by cell-to-cell transmission and aggregation of endogenous species in newly invaded neurons. Toxicity of α-syn PFF was investigated using primary cultures of dopaminergic neurons or on aged mice after infusion in the SNpc and combined with mild inhibition of GBA. In primary dopaminergic neurons, application of α-syn PFF induced a progressive cytotoxicity associated with mitochondrial dysfunction, oxidative stress, and accumulation of lysosomes suggesting that exogenous α-syn reached the lysosome (from the endosome). Counteracting the α-syn endocytosis with a clathrin inhibitor, dopaminergic neuron degeneration was prevented. In vivo, α-syn PFF induced progressive neurodegeneration of dopaminergic neurons associated with motor deficits. Histology revealed progressive aggregation of α-syn and microglial activation and accounted for the seeding role of α-syn, injection of which acted as a spark suggesting a triggering of cell-to-cell toxicity. We showed for the first time that a localized SNpc α-syn administration combined with a slight lysosomal deficiency and aging triggered a progressive lesion. The cellular and animal models described could help in the understanding of the human disease and might contribute to the development of new therapies.

show abstract

Cognitive Impairment in Parkinson’s Disease: Epidemiology, Clinical Profile, Protective and Risk Factors

Cited by 58 publications

References 182 publications

Effects of Pramipexole Combined with Nerve Growth Factor on Cognitive Impairment and Urinary AD7c-NTP Expression in Patients with Parkinson’s Disease

Effects of Pramipexole Combined with Nerve Growth Factor on Cognitive Impairment and Urinary AD7c-NTP Expression in Patients with Parkinson’s Disease

Spontaneous object exploration in a recessive gene knockout model of Parkinson’s disease: Development and progression of object recognition memory deficits in male Pink1-/- rats

Alpha-Synuclein: The Spark That Flames Dopaminergic Neurons, In Vitro and In Vivo Evidence

Contact Info

Product

Resources

About