A study based on the embodied emotion approach: The recognition of whole‐body social emotions and postural control in Alzheimer's disease dementia, Parkinson's disease and healthy control

The early stages of neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) involve deterioration of specific (visuo)motor functions. The aim of the current study was to investigate differences in visuomotor behavior between age-matched groups of 17 patients with AD, 17 patients with PD, and 20 healthy control subjects across three eye-hand-coordination tasks of different cognitive complexity. In two of three tasks, timing and execution parameters of eyes and hand significantly differed between groups. Timing and execution parameters of the eyes and hands could potentially give a quantitative description of disease specific deficits in the spatial and temporal domains and may serve as a tool to monitor disease progression in AD and PD populations.

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Dual task and postural control in Alzheimer's and Parkinson's disease

Motriz Revista de Educação Física ◽

10.1590/s1980-65742014000100012 ◽

2014 ◽

Vol 20 (1) ◽

pp. 78-84

Author(s):

Larissa Pires de Andrade ◽

Natália Madalena Rinaldi ◽

Flávia Gomes de Melo Coelho ◽

Kátia Tanaka ◽

Florindo Stella ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Postural Control ◽

Neurodegenerative Diseases ◽

Dual Task ◽

Center Of Pressure ◽

Cognitive Task ◽

Experimental Conditions

Patients with neurodegenerative diseases are required to use cognitive resources while maintaining postural control. The aim of this study was to investigate the effects of a frontal cognitive task on postural control in patients with Alzheimer, Parkinson and controls. Thirty-eight participants were instructed to stand upright on a force platform in two experimental conditions: single and dual task. Participants with Parkinson's disease presented an increase in the coefficient of variation greater than 100% in the dual task as compared to the single task for center of pressure (COP) area and COP path. In addition, patients with Parkinson's and Alzheimer's disease had a higher number of errors during the execution of the cognitive task when compared to the group of elderly without neurodegenerative diseases. The motor cortex, which is engaged in postural control, does not seem to compete with frontal brain regions in the performance of the cognitive task. However, patients with Parkinson's and Alzheimer's disease presented worsened performance in cognitive task.

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Formulaic Language in Parkinson's Disease and Alzheimer's Disease: Complementary Effects of Subcortical and Cortical Dysfunction

Journal of Speech Language and Hearing Research ◽

10.1044/2015_jslhr-l-14-0341 ◽

2015 ◽

Vol 58 (5) ◽

pp. 1493-1507 ◽

Cited By ~ 21

Author(s):

Diana Van Lancker Sidtis ◽

JiHee Choi ◽

Amy Alken ◽

John J. Sidtis

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Basal Ganglia ◽

Right Hemisphere ◽

Conversational Speech ◽

Formulaic Language ◽

Healthy Control ◽

The Right

Purpose The production of formulaic expressions (conversational speech formulas, pause fillers, idioms, and other fixed expressions) is excessive in the left hemisphere and deficient in the right hemisphere and in subcortical stroke. Speakers with Alzheimer's disease (AD), having functional basal ganglia, reveal abnormally high proportions of formulaic language. Persons with Parkinson's disease (PD), having dysfunctional basal ganglia, were predicted to show impoverished formulaic expressions in contrast to speakers with AD. This study compared participants with PD, participants with AD, and healthy control (HC) participants on protocols probing production and comprehension of formulaic expressions. Method Spontaneous speech samples were recorded from 16 individuals with PD, 12 individuals with AD, and 18 HC speakers. Structured tests were then administered as probes of comprehension. Results The PD group had lower proportions of formulaic expressions compared with the AD and HC groups. Comprehension testing yielded opposite contrasts: participants with PD showed significantly higher performance compared with participants with AD and did not differ from HC participants. Conclusions The finding that PD produced lower proportions of formulaic expressions compared with AD and HC supports the view that subcortical nuclei modulate the production of formulaic expressions. Contrasting results on formal testing of comprehension, whereby participants with AD performed significantly worse than participants with PD and HC participants, indicate differential effects on procedural and declarative knowledge associated with these neurological conditions.

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Cardiac sympathetic denervation and synucleinopathy in Alzheimer’s disease with brain Lewy body disease

Brain Communications ◽

10.1093/braincomms/fcaa004 ◽

2020 ◽

Vol 2 (1) ◽

Cited By ~ 2

Author(s):

Geidy E Serrano ◽

David Shprecher ◽

Michael Callan ◽

Brett Cutler ◽

Michael Glass ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Tyrosine Hydroxylase ◽

Lewy Body ◽

Dementia With Lewy Bodies ◽

Lewy Bodies ◽

Alpha Synuclein ◽

Alzheimer’S Disease Dementia

Abstract Comorbid Lewy body pathology is very common in Alzheimer’s disease and may confound clinical trial design, yet there is no in vivo test to identify patients with this. Tissue (and/or radioligand imaging) studies have shown cardiac sympathetic denervation in Parkinson’s disease and dementia with Lewy bodies, but this has not been explored in Alzheimer’s subjects with Lewy bodies not meeting dementia with Lewy bodies clinicopathological criteria. To determine if Alzheimer’s disease with Lewy bodies subjects show sympathetic cardiac denervation, we analysed epicardial and myocardial tissue from autopsy-confirmed cases using tyrosine hydroxylase and neurofilament immunostaining. Comparison of tyrosine hydroxylase fibre density in 19 subjects with Alzheimer’s disease/dementia with Lewy bodies, 20 Alzheimer’s disease with Lewy bodies, 12 Alzheimer’s disease subjects without Lewy body disease, 19 Parkinson’s disease, 30 incidental Lewy body disease and 22 cognitively normal without Alzheimer’s disease or Lewy body disease indicated a significant group difference (P < 0.01; Kruskal–Wallis analysis of variance) and subsequent pair-wise Mann–Whitney U tests showed that Parkinson’s disease (P < 0.05) and Alzheimer’s disease/dementia with Lewy bodies (P < 0.01) subjects, but not Alzheimer’s disease with Lewy bodies subjects, had significantly reduced tyrosine hydroxylase fibre density as compared with cognitively normal. Both Parkinson’s disease and Alzheimer’s disease/dementia with Lewy bodies subjects also showed significant epicardial losses of neurofilament protein-immunoreactive nerve fibre densities within the fibre bundles as compared with cognitively normal subjects (P < 0.01) and both groups showed high pathologic alpha-synuclein densities (P < 0.0001). Cardiac alpha-synuclein densities correlated significantly with brain alpha-synuclein (P < 0.001), while cardiac tyrosine hydroxylase and neurofilament immunoreactive nerve fibre densities were negatively correlated with the densities of both brain and cardiac alpha-synuclein, as well as Unified Parkinson’s Disease Rating Scale scores (P < 0.05). The clear separation of Alzheimer’s disease/dementia with Lewy bodies subjects from Alzheimer’s disease and cognitively normal, based on cardiac tyrosine hydroxylase fibre density, is the first report of a statistically significant difference between these groups. Our data do not show significant sympathetic cardiac denervation in Alzheimer’s disease with Lewy bodies, but strongly confirm that cardiac nuclear imaging with a noradrenergic radioligand is worthy of further study as a potential means to separate Alzheimer’s disease from Alzheimer’s disease/dementia with Lewy bodies during life.

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P2-370: Different patterns of cerebral cortical hypoperfusion by IMP-SPECT and stereotactic extraction estimation method in Alzheimer's disease, dementia with Lewy bodies, and Parkinson's disease with dementia

Alzheimer s & Dementia ◽

10.1016/j.jalz.2010.05.1422 ◽

2010 ◽

Vol 6 ◽

pp. S423-S423

Author(s):

Kouichi Ohta ◽

Morinobu Seki ◽

Yukito Shinohara

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Dementia With Lewy Bodies ◽

Estimation Method ◽

Lewy Bodies ◽

Parkinson’S Disease With Dementia ◽

Alzheimer’S Disease Dementia

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Widespread Decreases in Cerebral Copper Are Common to Parkinson's Disease Dementia and Alzheimer's Disease Dementia

Frontiers in Aging Neuroscience ◽

10.3389/fnagi.2021.641222 ◽

2021 ◽

Vol 13 ◽

Author(s):

Melissa Scholefield ◽

Stephanie J. Church ◽

Jingshu Xu ◽

Stefano Patassini ◽

Federico Roncaroli ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Primary Motor Cortex ◽

Middle Temporal Gyrus ◽

Essential Metals ◽

Parkinson’S Disease Dementia ◽

Metal Levels ◽

Alzheimer’S Disease Dementia

Several studies of Parkinson's disease (PD) have reported dysregulation of cerebral metals, particularly decreases in copper and increases in iron in substantia nigra (SN). However, few studies have investigated regions outside the SN, fewer have measured levels of multiple metals across different regions within the same brains, and there are no currently-available reports of metal levels in Parkinson's disease dementia (PDD). This study aimed to compare concentrations of nine essential metals across nine different brain regions in cases of PDD and controls. Investigated were: primary motor cortex (MCX); cingulate gyrus (CG); primary visual cortex (PVC); hippocampus (HP); cerebellar cortex (CB); SN; locus coeruleus (LC); medulla oblongata (MED); and middle temporal gyrus (MTG), thus covering regions with severe, moderate, or low levels of neuronal loss in PDD. Levels of eight essential metals and selenium were determined using an analytical methodology involving the use of inductively-coupled plasma mass spectrometry (ICP-MS), and compared between cases and controls, to better understand the extent and severity of metal perturbations. Findings were also compared with those from our previous study of sporadic Alzheimer's disease dementia (ADD), which employed equivalent methods, to identify differences and similarities between these conditions. Widespread copper decreases occurred in PDD in seven of nine regions (exceptions being LC and CB). Four PDD-affected regions showed similar decreases in ADD: CG, HP, MTG, and MCX. Decreases in potassium and manganese were present in HP, MTG and MCX; decreased manganese was also found in SN and MED. Decreased selenium and magnesium were present in MCX, and decreased zinc in HP. There was no evidence for increased iron in SN or any other region. These results identify alterations in levels of several metals across multiple regions of PDD brain, the commonest being widespread decreases in copper that closely resemble those in ADD, pointing to similar disease mechanisms in both dementias.

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Neurobehavioral Consequences Associated with Long Term Tramadol Utilization and Pathological Mechanisms

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527318666191112124435 ◽

2020 ◽

Vol 18 (10) ◽

pp. 758-768 ◽

Cited By ~ 2

Author(s):

Khadga Raj ◽

Pooja Chawla ◽

Shamsher Singh

Keyword(s):

Alzheimer’S Disease ◽

Parkinson’S Disease ◽

Alzheimer's Disease ◽

Parkinson's Disease ◽

Serotonin Reuptake ◽

Selective Serotonin Reuptake Inhibitors ◽

Serotonin Syndrome ◽

Dopamine Synthesis ◽

Synthetic Analog

: Tramadol is a synthetic analog of codeine used to treat pain of moderate to severe intensity and is reported to have neurotoxic potential. At therapeutic dose, tramadol does not cause major side effects in comparison to other opioid analgesics, and is useful for the management of neurological problems like anxiety and depression. Long term utilization of tramadol is associated with various neurological disorders like seizures, serotonin syndrome, Alzheimer’s disease and Parkinson’s disease. Tramadol produces seizures through inhibition of nitric oxide, serotonin reuptake and inhibitory effects on GABA receptors. Extensive tramadol intake alters redox balance through elevating lipid peroxidation and free radical leading to neurotoxicity and produces neurobehavioral deficits. During Alzheimer’s disease progression, low level of intracellular signalling molecules like cGMP, cAMP, PKC and PKA affect both learning and memory. Pharmacologically tramadol produces actions similar to Selective Serotonin Reuptake Inhibitors (SSRIs), increasing the concentration of serotonin, which causes serotonin syndrome. In addition, tramadol also inhibits GABAA receptors in the CNS has been evidenced to interfere with dopamine synthesis and release, responsible for motor symptoms. The reduced level of dopamine may produce bradykinesia and tremors which are chief motor abnormalities in Parkinson’s Disease (PD).

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