← Back to all signals
RESEARCH PAPER ANALYSIS

The clock drawing test as a screening tool for detecting cognitive decline: an analysis in adults and elderly people from Natal (RN).

In 113 adults from Northeastern Brazil, Shulman's Clock Drawing Test showed limited overall sensitivity and accuracy, was affected by age and low education, had high sensitivity for major neurocognitive disorder due to Alzheimer's, moderate sensitivity for non‑AD major NCDs (including Parkinson's…

PMID41959610
JournalFrontiers in human neuroscience
Publication Date2026-01-01
Ingested2026-04-28 08:58 PM
EXECUTIVE SUMMARY

What the AI sees

In 113 adults from Northeastern Brazil, Shulman's Clock Drawing Test showed limited overall sensitivity and accuracy, was affected by age and low education, had high sensitivity for major neurocognitive disorder due to Alzheimer's, moderate sensitivity for non‑AD major NCDs (including Parkinson's…

WHY IT MATTERS

Research significance

This paper provides little direct value for Parkinson's therapeutic discovery because it offers no mechanistic or biomarker targets, but its note that CDT has moderate sensitivity for Parkinson's-related major neurocognitive disorder may inform clinical screening or cohort selection in dementia…

ABSTRACT

Source abstract

INTRODUCTION: The Clock Drawing Test (CDT) is widely used as a screening instrument for cognitive decline due to its simplicity and rapid administration. Despite its widespread clinical use, evidence regarding its diagnostic performance in the Brazilian Northeast region remains scarce. METHODS: This study examined CDT performance in a clinical sample of 113 adults and older adults assessed at a neuropsychology service in Northeastern Brazil, focusing on CDT ability to identify cognitive decline and the effects of age, educational level, and clinical diagnoses. The study tested the following hypotheses: (1) there is a significant association between age and CDT scores; (2) there are significant differences in CDT scores across different educational levels; (3) there are significant differences in CDT scores across different clinical conditions, indicating potential for differential diagnosis; and (4) the test would demonstrate high sensitivity, specificity, and accuracy in the overall sample, as well as high sensitivity in detecting each diagnostic condition. Using Shulman's scoring method, descriptive analyses, Spearman's correlation, Kruskal-Wallis tests and metrics of sensitivity, specificity, and accuracy were conducted. RESULTS: The sample had a mean age of 65.19 years and was predominantly characterized by low educational attainment. A negative, albeit weak, correlation was observed between age and CDT scores, as well as significant differences across educational levels. Diagnostic group comparisons also revealed significant differences, most notably between cognitively unimpaired individuals and patients diagnosed with Major Neurocognitive Disorder due to Alzheimer's disease. Although the CDT demonstrated adequate specificity, its overall sensitivity and accuracy were low. Sensitivity was high for Major Neurocognitive Disorder Due to Alzheimer's Disease, moderate for Major Neurocognitive Disorder due to Non-Alzheimer's Disease (Major Vascular Neurocognitive Disorder, Parkinson's Disease, Mixed Dementia, Wernicke-Korsakoff syndrome and Major Frontotemporal Neurocognitive Disorder) and low for Mild Neurocognitive Disorder. DISCUSSION: These findings demonstrate that Shulman's method of CDT is not suitable for assessing cognitive decline in the illiterate and low-education population and raise important concerns regarding its standalone clinical utility, especially in specific neurological conditions. The present study underscores the need for future research employing alternative scoring methods and more representative samples to refine the applicability and diagnostic value of the CDT in clinical practice.

SUPPORTING PAPER SET

32 more papers to review

Ranked by current scoring engine
1 The cGAS-STING-Glymphatic-gut Axis in Parkinson's disease: A proposed self-amplifying triad of Neuroinflammation and therapeutic opportunity. International immunopharmacology 91.0 2 Immunosenescence and Inflammaging as Drivers of Neurodegeneration: Cellular Mechanisms, Neuroimmune Crosstalk, and Therapeutic Implications. Cells 91.0 3 Flavonoids improve neurotransmitters for Parkinson's treatment: mechanism and therapeutic potential. Frontiers in pharmacology 88.0 4 Alpha-Lipoic Acid and Biotin in Neurodegenerative Diseases: Convergent Mechanistic Insights from Preclinical Models to Clinical Perspectives. Neurology international 78.0 5 The Gut Microbiota in Parkinson's Disease: Mechanistic Insights into Microbial-Host Interactions. Microorganisms 85.0 6 Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes. Frontiers in clinical diabetes and healthcare 80.0 7 Neuroprotective effects of GLP-2 and a GLP-2/GIP dual receptor agonist in an MPTP-induced mouse model of Parkinson's disease. Peptides 86.0 8 TNF alpha unmasks enteric malate aspartate shuttle dysfunction bridging Parkinson disease and intestinal inflammation. Nature communications 91.5 9 Lipid Metabolism and Neurodegeneration: Mechanistic Insights and Therapeutic Targets. Ageing research reviews 82.0 10 Shared functional microbiome signatures in Parkinson's disease and constipation predominate irritable bowel syndrome despite taxonomic divergence. Brain, behavior, & immunity - health 80.0 11 Benzimidazole as a Versatile Scaffold for Developing Neurotherapeutics Against Neurodegenerative Diseases. ChemMedChem 74.0 12 Biomimicking neuromelanin reverses the gait deficits and dopaminergic neuronal loss in the Parkinson's disease. Colloids and surfaces. B, Biointerfaces 86.0 13 Neuroprotective roles of klotho: Molecular pathways and therapeutic implications for cognitive health in neurological and psychiatric diseases. Experimental physiology 84.0 14 Flavonoid Rutin Reduces Intestinal Inflammation in an Experimental Model of Parkinson's Disease. Neurotoxicity research 70.0 15 Nanostructured Lipid Carriers Enhance Brain Delivery and Antioxidant Efficacy of a Small-Molecule MAO B Inhibitor for Neurodegenerative Disease Therapy. Molecular pharmaceutics 78.0 16 Pathophysiological Role of the Gut Brain Axis in Parkinson's Disease: From Microbial Metabolites and Intestinal Permeability to Central Neuroinflammation. Current neurovascular research 86.0 17 Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review. Current issues in molecular biology 86.0 18 Navigating the cholesterol maze: Key insights on use of statins in neurodegenerative disorders. Neuroprotection (Chichester, England) 76.0 19 Integrative network pharmacology delineates dual GPCR and non-GPCR mechanisms of blended and individual Taikong Blue lavender and Pingyin rose essential oils in neurodegenerative and psychiatric disorders. Computers in biology and medicine 65.0 20 Models of neuroprotection in Parkinson's disease: Exploring cellular, molecular, and microenvironmental targets. Experimental neurology 78.0 21 Hyaluronic acid: emerging roles and biomaterial innovations in Alzheimer's and Parkinson's disease therapy. Frontiers in pharmacology 75.2 22 Molecular mechanisms underlying Parkinson's disease and role of phytochemicals, α-synuclein, sirtuins, and incretin mimetics in potential therapy. Frontiers in pharmacology 75.0 23 Lipid droplets in neurodegenerative diseases: pathological drivers and therapeutic vulnerabilities. Cell death discovery 82.0 24 Brain-gut-microbiota axis: a review on the bidirectional regulatory mechanisms between gut microbiota and brain and their disease interactions. Frontiers in microbiology 74.0 25 Long non-coding RNAs in neurodegenerative diseases - Molecular mechanisms, liquid biopsy biomarkers, and therapeutic targets: A review. Biomolecules & biomedicine 84.0 26 Neurosyphilis and Parkinsonism: Overlapping Pathophysiology and Emerging Therapeutic Insights. Current neurovascular research 76.0 27 Molecular biochemistry of soluble epoxide hydrolase in lipid mediator pathways and neuroinflammatory responses. The Journal of steroid biochemistry and molecular biology 82.0 28 Multifaceted role of CNPY2 beyond ER stress: Disease implications and therapeutic potential. Cell stress 83.3 29 Neuroprotective Role of Exercise-based Physiotherapy Combined with Pharmacological Agents in Parkinson's Disease. Central nervous system agents in medicinal chemistry 64.0 30 Distinct metabolomic and proteomic signatures in Parkinson's disease patients with REM sleep behavior disorder. Signal transduction and targeted therapy 84.0 31 HMGB1-mediated neuroinflammation: molecular mechanisms and emerging therapeutic approaches. Inflammopharmacology 78.0 32 Beyond acid-base dyshomeostasis: Dynamic instability of neuronal lysosomal pH as a pathogenic mechanism and therapeutic target in neurological diseases. Biochemical pharmacology 88.0
Neurocompute Parkinson’s Narrative Velocity Infographic
NEUROCOMPUTE VISUAL SYSTEM

Open the Narrative Velocity Map

Explore the full Parkinson’s research intelligence diagram.

Expand Intelligence View →
Full Neurocompute Infographic