Block Duration in Session 1 (A) and Session 2 (B).

<p>Data points represent group means for each block and error bars depict standard errors. Black squares = healthy controls; blue circles = left hand asymptomatic (LH-A) patients with PD; red crosses = left hand symptomatic patients (LH-S) with PD. Thick solid lines represent group-averaged trajectories based on a single exponential fit.</p

Experimental Design.

<p>See text for details of each phase. W/U = warm-up.</p

Participant characteristics.

<p>Values are means ± SD. MMSE = Mini Mental State Examination; GDS = Geriatric Depression Scale; UPDRS = Unified Parkinson’s Disease Rating Scale. L-UPDRS III = left side scores of UPDRS part III; R-UPDRS III = right side scores of UPDRS part III. PIGD = postural instability—gait difficulty. PD-dominance was based on method employed in [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0134291#pone.0134291.ref044" target="_blank">44</a>].</p><p>Participant characteristics.</p

Motor Sequence Learning and Consolidation in Unilateral <i>De Novo</i> Patients with Parkinson’s Disease

<div><p>Previous research investigating motor sequence learning (MSL) and consolidation in patients with Parkinson’s disease (PD) has predominantly included heterogeneous participant samples with early and advanced disease stages; thus, little is known about the onset of potential behavioral impairments. We employed a multisession MSL paradigm to investigate whether behavioral deficits in learning and consolidation appear immediately after or prior to the detection of clinical symptoms in the tested (left) hand. Specifically, our patient sample was limited to recently diagnosed patients with pure unilateral PD. The left hand symptomatic (LH-S) patients provided an assessment of performance following the onset of clinical symptoms in the tested hand. Conversely, right hand affected (left hand asymptomatic, LH-A) patients served to investigate whether MSL impairments appear before symptoms in the tested hand. LH-S patients demonstrated impaired learning during the initial training session and both LH-S and LH-A patients demonstrated decreased performance compared to controls during the next-day retest. Critically, the impairments in later learning stages in the LH-A patients were evident even before the appearance of traditional clinical symptoms in the tested hand. Results may be explained by the progression of disease-related alterations in relevant corticostriatal networks.</p></div

Performance Index (PI) in Session 1 (A) and Session 2 (B).

<p>Data points represent group means for each block and error bars depict standard errors. Black squares = healthy controls; blue circles = left hand asymptomatic (LH-A) patients with PD; red crosses = left hand symptomatic patients (LH-S) with PD. Thick solid lines represent group-averaged trajectories based on a single exponential fit.</p

Additional file 2: Table S2. of The prevalence and incidence of frailty in Pre-diabetic and diabetic community-dwelling older population: results from Beijing longitudinal study of aging II (BLSA-II)

Odds ratios and relative risks of frailty comparing pre-diabetic and diabetic subjects with those with normal blood glucose at baseline and follow-up visits. (DOCX 29 kb

Table_1_Parkinson's disease and comorbid myasthenia gravis: a case report and literature review.docx

BackgroundParkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. Myasthenia gravis (MG) is a rare autoimmune disease caused by antibodies against the neuromuscular junction. PD and comorbid MG are rarely seen.Case presentationHere we report on a patient who was diagnosed with PD and MG. A 74-year-old man had a 4-year history of bradykinesia and was diagnosed with PD. He subsequently developed incomplete palpebral ptosis, apparent dropped head, and shuffling of gait. The results of neostigmine tests were positive. Repetitive nerve stimulation (RNS) showed significant decremental responses at 3 and 5 Hz in the orbicularis oculi. The patient's anti-acetylcholine receptor (anti-AchR) antibody serum level was also elevated. Meanwhile, 9-[18F]fluoropropyl-(+)-dihydrotetrabenazine positron emission tomography–computed tomography (18F-AV133 PET-CT) scan revealed a significant decrease in uptake in the bilateral putamen. After addition of cholinesterase inhibitors, his symptoms of palpebral ptosis and head drop improved greatly and he showed a good response to levodopa.ConclusionAlthough PD with MG is rare, we still need to notice the possibility that a PD patient may have comorbid MG. The underlying mechanism of PD and comorbid MG remains unknown, but an imbalance between the neurotransmitters dopamine and acetylcholine and the immune system are likely to play significant roles in the pathogenesis. In this article, we present our case and a literature review on the co-occurrence of PD and MG, reviewing their clinical features, and discuss the underlying pathogenic mechanism of this comorbidity.</p

Lack of correlation between individual patients’ task performance and clinical data.

<p>Test scores and ordering costs were from the DOT-A. The values were mean-corrected and age-/education-adjusted.</p

Test scores and ordering costs.

<p>(A) Mean test scores and standard errors of the adaptive digit ordering test (DOT-A), digit span forward (Forw) and backward tests (Backw) in mild PD patients with normal global cognition (PD-NC) or with mild cognitive impairment (PD-MCI) and in healthy controls (HC). The mean values were adjusted to 63.9 years of age and 12.8 years of education. Asterisks (*) indicate significant differences between patients and controls (<i>p</i><0.05). (B) Mean ordering costs and standard errors of the DOT-A and backward test in each group. The mean values were age- and education-adjusted. Asterisks indicate significant differences between patients and controls. (C) The DOT-A ordering cost increased in older adults across groups. The values were mean-corrected. (D) Difference between the DOT-A ordering cost and backward ordering cost decreased in older adults across groups. The values were mean-corrected.</p

Video_1_Parkinson's disease and comorbid myasthenia gravis: a case report and literature review.MP4

BackgroundParkinson's disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. Myasthenia gravis (MG) is a rare autoimmune disease caused by antibodies against the neuromuscular junction. PD and comorbid MG are rarely seen.Case presentationHere we report on a patient who was diagnosed with PD and MG. A 74-year-old man had a 4-year history of bradykinesia and was diagnosed with PD. He subsequently developed incomplete palpebral ptosis, apparent dropped head, and shuffling of gait. The results of neostigmine tests were positive. Repetitive nerve stimulation (RNS) showed significant decremental responses at 3 and 5 Hz in the orbicularis oculi. The patient's anti-acetylcholine receptor (anti-AchR) antibody serum level was also elevated. Meanwhile, 9-[18F]fluoropropyl-(+)-dihydrotetrabenazine positron emission tomography–computed tomography (18F-AV133 PET-CT) scan revealed a significant decrease in uptake in the bilateral putamen. After addition of cholinesterase inhibitors, his symptoms of palpebral ptosis and head drop improved greatly and he showed a good response to levodopa.ConclusionAlthough PD with MG is rare, we still need to notice the possibility that a PD patient may have comorbid MG. The underlying mechanism of PD and comorbid MG remains unknown, but an imbalance between the neurotransmitters dopamine and acetylcholine and the immune system are likely to play significant roles in the pathogenesis. In this article, we present our case and a literature review on the co-occurrence of PD and MG, reviewing their clinical features, and discuss the underlying pathogenic mechanism of this comorbidity.</p