Background: Brain magnetic resonance imaging (MRI) allows researchers to observe structural pathology that may predict cognitive decline. Some populations are less accessible through traditional in-person visits, and may be under-represented in the literature.
Methods: We examined white matter hyperintensity volume (WMHV) and cerebral parenchymal fraction (CPF) as predictors of cognitive decline measured by a modified Telephone Interview for Cognitive Status (TICS-m) in the Northern Manhattan Stroke Study, a racially and ethnically diverse cohort study. Participants were stroke-free, above 50 years old, and had no contraindications to MRI. A total of 1143 participants had MRI and TICS-m data available [mean age 70 (SD=9), 61% women, 66% Hispanic, 17% Black, 15% white].
Results: Those in the third and fourth quartiles of WMHV had significantly greater decline in TICS-m over time as compared with those in the first quartile (Q3: -0.17 points/year, Q4: -0.30 points/year). Those in the bottom 2 quartiles of CPF had significantly greater decline in TICS-m than those in the top quartile (Q1: -0.3 points/year, Q2: -0.2 points/year). Apolipoprotein E (APOE) e4 allele carriers had greater cognitive decline per unit of CPF. Those with greater CPF preserve TICS-m performance better despite greater WMHV.
Conclusions: Telephone cognitive assessments can detect decline due to white matter lesions and smaller brain volumes.
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http://dx.doi.org/10.1097/WAD.0000000000000158 | DOI Listing |
Brain Behav Immun Health
February 2025
Department of Physiology, School of Medicine, University College Cork, Western Road, Cork, Ireland.
Duchenne muscular dystrophy (DMD), an X-linked neuromuscular disorder, characterised by progressive immobility, chronic inflammation and premature death, is caused by the loss of the mechano-transducing signalling molecule, dystrophin. In non-contracting cells, such as neurons, dystrophin is likely to have a functional role in synaptic plasticity, anchoring post-synaptic receptors. Dystrophin-expressing hippocampal neurons are key to cognitive functions such as emotions, learning and the consolidation of memories.
View Article and Find Full Text PDFBrain Behav Immun Health
February 2025
Department of Neurology, Vagelos College of Physicians and Surgeons, Columbia University, New York, NY, USA.
Objective: To determine whether a panel of immune markers adds significant information to known correlates of risk of dementia and cognitive impairment.
Background: The impact of immune mechanisms on dementia risk is incompletely characterized.
Design/methods: A subsample of the Northern Manhattan Study, a prospective cohort study in the racially/ethnically diverse population of New York City, underwent comprehensive neuropsychological testing up to three times, at approximately 5-year intervals.
Schizophr Res Cogn
June 2025
University Department of Child and Adolescent Psychiatry, Children's Hospitals of NICE CHU-Lenval, Nice, France.
Objective: To conduct a systematic review of neurocognitive dysfunctions in patients with childhood-onset schizophrenia (COS), a neuropsychiatric disorder that occurs before age 13 and is rarer and more severe than adult-onset schizophrenia.
Method: A search was made in the PubMed database. Sixty-seven studies (out of 543) which analyzed Intellectual Quotient (IQ), attentional, memory and executive functions were selected by two independent researchers.
Front Nutr
January 2025
College of Food Science and Technology, Yunan Agricultural University, Kunming, China.
Diabetic cognitive dysfunction is one of the important comorbidities and complications of diabetes, which is mainly manifested by loss of learning ability and memory, behavioural disorders, and may even develop into dementia. While traditional anti-diabetic medications are effective in improving cognition and memory, long-term use of these medications can be accompanied by undesirable side effects. Therefore, there is an urgent need to find safe and effective alternative therapies.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Neurophysiology, Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez", Mexico City, Mexico.
The interplay between long-term potentiation (LTP) and epilepsy represents a crucial facet in understanding synaptic plasticity and memory within neuroscience. LTP, a phenomenon characterized by a sustained increase in synaptic strength, is pivotal in learning and memory processes, particularly in the hippocampus. This review delves into the intricate relationship between LTP and epilepsy, exploring how alterations in synaptic plasticity mechanisms akin to those seen in LTP contribute to the hyperexcitable state of epilepsy.
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