Visuospatial Judgment

Benton, Arthur L.

doi:10.1001/archneur.1978.00500300038006

Cited by 879 publications

(408 citation statements)

References 12 publications

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“…Global cognition was assessed with the MoCA 6, 7. Cognitive testing included the Hopkins Verbal Learning Test‐Revised (HLVT‐R) to assess memory; Benton Judgment of Line Orientation (JOLO) 15‐item version to assess visuospatial function; Symbol‐Digit Modalities Test (SDMT) to assess processing speed‐attention; and Letter‐Number Sequencing (LNS) and semantic (animal) fluency to assess executive abilities‐working memory 8, 9, 10, 11, 12. Published norms were applied.…”

Section: Methodsmentioning

confidence: 99%

The Parkinson's progression markers initiative (PPMI) – establishing a PD biomarker cohort

Marek

Chowdhury

Siderowf

et al. 2018

Ann Clin Transl Neurol

397

339

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ObjectiveThe Parkinson's Progression Markers Initiative (PPMI) is an observational, international study designed to establish biomarker‐defined cohorts and identify clinical, imaging, genetic, and biospecimen Parkinson's disease (PD) progression markers to accelerate disease‐modifying therapeutic trials.MethodsA total of 423 untreated PD, 196 Healthy Control (HC) and 64 SWEDD (scans without evidence of dopaminergic deficit) subjects were enrolled at 24 sites. To enroll PD subjects as early as possible following diagnosis, subjects were eligible with only asymmetric bradykinesia or tremor plus a dopamine transporter (DAT) binding deficit on SPECT imaging. Acquisition of data was standardized as detailed at www.ppmi-info.org.ResultsApproximately 9% of enrolled subjects had a single PD sign at baseline. DAT imaging excluded 16% of potential PD subjects with SWEDD. The total MDS‐UPDRS for PD was 32.4 compared to 4.6 for HC and 28.2 for SWEDD. On average, PD subjects demonstrated 45% and 68% reduction in mean striatal and contralateral putamen Specific Binding Ratios (SBR), respectively. Cerebrospinal fluid (CSF) was acquired from >97% of all subjects. CSF (PD/HC/SWEDD pg/mL) α‐synuclein (1845/2204/2141) was reduced in PD vs HC or SWEDD (P < 0.03). Similarly, t‐tau (45/53) and p‐tau (16/18) were reduced in PD versus HC (P < 0.01),Interpretation PPMI has detailed the biomarker signature for an early PD cohort defined by clinical features and imaging biomarkers. This strategy provides the framework to establish biomarker cohorts and to define longitudinal progression biomarkers to support future PD treatment trials.

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Section: Methodsmentioning

confidence: 99%

The Parkinson's progression markers initiative (PPMI) – establishing a PD biomarker cohort

Marek

Chowdhury

Siderowf

et al. 2018

Ann Clin Transl Neurol

397

339

View full text Add to dashboard Cite

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“…The evaluation included a medical history and interview for common problems of older persons, a complete neurological examination, and a battery of cognitive tests chosen to measure a range of cognitive abilities with emphasis on those affected by aging and AD. [42][43][44][45][46][47][48][49] A board-certified neuropsychologist, blinded to age, sex, race/ethnicity, and clinical data other than occupation, education, and information about motor or sensory deficits and effort, used these results to summarize impairment in each of the five cognitive domains (orientation, attention, memory, language, and perception 50,51 ), scoring them as not present, possible, or probable. After the review of all clinical data from that year and examination of the participant, a clinical diagnosis was made.…”

Section: Clinical Evaluationmentioning

confidence: 99%

Progression of Tau Pathology in Cholinergic Basal Forebrain Neurons in Mild Cognitive Impairment and Alzheimer's Disease

Vana

Kanaan

Ugwu

et al. 2011

The American Journal of Pathology

109

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Tau is a microtubule-associated protein that forms neurofibrillary tangles (NFTs) in the selective vulnerable long projection neurons of the cholinergic basal forebrain (CBF) in Alzheimer's disease (AD). Although CBF neurodegeneration correlates with cognitive decline during AD progression, little is known about the temporal changes of tau accumulation in this region. We investigated tau posttranslational modifications during NFT evolution within the CBF neurons of the nucleus basalis (NB) using tissue from subjects with no cognitive impairment, mild cognitive impairment, and AD. The pS422 antibody was used as an early tau pathology marker that labels tau phosphorylated at Ser422; the TauC3 antibody was used to detect later stage tau pathology. Stereologic evaluation of NB tissue immunostained for pS422 and TauC3 revealed an increase in neurons expressing these tau epitopes during disease progression. We also investigated the occurrence of pretangle tau events within cholinergic NB neurons by dual staining for the cholinergic cell marker, p75 NTR , which displays a phenotypic down-regulation within CBF perikarya in AD. As pS422؉ neurons increased in number, p75 NTR ؉ neurons decreased, and these changes correlated with both AD neuropathology and cognitive decline. Also, NFTs developed slower in the CBF compared with previously examined cortical regions. Taken together, these results suggest that changes in cognition are associated with pretangle events within NB cholinergic neurons before frank Degeneration of the cholinergic basal forebrain (CBF) neurons, which provide the major cholinergic innervation to the entire cortical mantle, hippocampus, and amygdala 1,2 correlates with dementia severity, disease duration, and cognitive impairment 3,4 in Alzheimer's disease (AD). 3,5-9 The viability of CBF neurons is dependent on the prototypic neurotrophic substance, nerve growth factor (NGF), 10 which is retrogradely transported to CBF neurons through a complex interaction of its two receptors, the high-affinity NGF-specific cell survival tyrosine kinase (trkA) and the putative cell death associated lowaffinity pan neurotrophin (p75 NTR ) receptor. 11,12 Previous studies have identified critical changes within the basocortical cholinergic system during the progression of AD, indicating a shift in the balance from pro-survival to apoptotic mechanisms, before frank cellular alteration, 13,14 which likely over time plays a mechanistic role in the CBF degeneration seen in AD. 5 In addition to altered neurotrophic factor dysfunction coincident with disease progression, CBF neurons also develop intracellular inclusions that appear as globose neurofibrillary tangles (NFTs) and neuropil threads (NTs), hallmark tau pathologies found in AD. [15][16][17] Tau is a microtubule-associated protein involved in normal cytoskeleton function, 18,19 but in AD tau transitions from its relatively soluble state into filamentous aggregates. 20 Braak and colleagues delineated six stages (I to VI) related to the spatial temporal distribution a...

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“…prefrontal cortex, occipital cortex and hippocampus). (Benton et al 1978): the JoLO requires subjects to identify which two of 11 lines presented in a semicircular array have the same orientation in a two-dimensional space as two target lines. The original JoLO was made more difficult to reduce its ceiling effect and to increase its sensitivity to brain dysfunction.…”

Section: Neuropsychological Assessmentsmentioning

confidence: 99%

Long-term neuropsychological effects of ecstasy in middle-aged ecstasy/polydrug users

et al. 2009

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Rationale Studies reporting ecstasy-induced serotonintoxicity and (neuro)psychological dysfunctions have been conducted in young adults. Little is known about ecstasy effects later in life, when serotonin levels and cognition decrease as a consequence of normal ageing. Objective This study aimed to assess whether harmful effects of ecstasy only add to or also interact with agerelated neuropsychological decline. Methods Attention, verbal and visual memory, visuospatial ability, self-reported depression, sensation-seeking and impulsivity were assessed in middle-aged moderate to heavy ecstasy/polydrug users (n=17) and compared with none or very mild ecstasy using polydrug users (matched for age, gender, intelligence and other drugs; n=16) and a group of drug-naive controls (n=20). Results Moderate to heavy ecstasy/polydrug users performed significantly worse on a verbal memory task than none or very mild ecstasy using polydrug users and drug naives. Moderate and heavy ecstasy/polydrug users also differed significantly from drug-naives on measures of depression, sensation-seeking and impulsivity but not from none or very mild ecstasy-using polydrug users. Conclusion This study in middle-aged ecstasy/polydrug users replicated findings of studies in younger ecstasy users, showing a harmful effect of ecstasy on verbal memory. There was no clear support for an interaction between harmful effects of ecstasy use and age-related memory decline or mid-life depression.

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Visuospatial Judgment

Cited by 879 publications

References 12 publications

The Parkinson's progression markers initiative (PPMI) – establishing a PD biomarker cohort

The Parkinson's progression markers initiative (PPMI) – establishing a PD biomarker cohort

Progression of Tau Pathology in Cholinergic Basal Forebrain Neurons in Mild Cognitive Impairment and Alzheimer's Disease

Long-term neuropsychological effects of ecstasy in middle-aged ecstasy/polydrug users

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