Studies with human and animal subjects have indicated age declines in short-term memory and cell loss in the cortex. Cell loss has been estamated by descriptive nonautomated methods. Declines in short-term memory may be related to reduced learning, movtivation, motor capacity, or some combination of these factors. Passive-avoidance tests of memory minimize these factors. Direct correlational studies on learning and memory in relation to cell loss in the same subject are not feasible in man and they have not been reported previously in animals. The aims of this study were to examine age differences in learning and short-term passive-avoidance memory in relation to cell packing density in the visual cortex of the Fisher 344 rat. Cell counts were made with a computer-guided, automated, image-analyzing system (TAS, Leitz). The following observations were made: (1) significant age differences in 2- and 6-hour short-term passive-avoidance retention or memory between mature and senescent rats were related to nonsignificant age differences in original learning inferred from starting latencies, running time and running distance and (2) sd compared to mature rats were associated with significant differences in neuron but not glia-vascular cell density in area 17 in the presence of nonsignificant age differences in cortical depth and brain weight. Aims of further studies are to establish the role of cell loss from the hippocampus in loss of short-term spatial memory with age and to develop criteria for differential counting of small neurons, glia, endothelial cells and pericytes.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1159/000212260 | DOI Listing |
Alzheimers Dement
December 2024
University of North Carolina Gillings School of Global Public Health, Chapel Hill, NC, USA.
Background: Pharmacoepidemiologic studies assessing drug effectiveness for Alzheimer's disease and related dementias (ADRD) are increasingly popular given the critical need for effective therapies for ADRD. To meet the urgent need for robust dementia ascertainment from real-world data, we aimed to develop a novel algorithm for identifying incident and prevalent dementia in claims.
Method: We developed algorithm candidates by different timing/frequency of dementia diagnosis/treatment to identify dementia from inpatient/outpatient/prescription claims for 6,515 and 3,997 participants from Visits 5 (2011-2013; mean age 75.
Alzheimers Dement
December 2024
Innovation Center for Neurological Disorders and Department of Neurology, Xuanwu Hospital, Capital Medical University, Beijing, Beijing, China.
Background: The DL-3-n-butylphthalide (NBP), a multi-target neuroprotective drug, improving cognitive impairment in patient with vascular cognitive impairment has been confirmed. The efficacy of NBP in patients with cognitive impairment due to Alzheimer's disease (AD) remains unknown. This study aimed to evaluate the efficacy and safety of NBP in patients with mild cognitive impairment (MCI) due to AD though a clinical randomized controlled trail.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Loma Linda University Health, Loma Linda, CA, USA.
Background: Only about 50% of the variance in cognitive decline occurring during Alzheimer's pathogenesis is attributable to standard AD biomarkers (cerebrocortical Aβ, pathological tau, and atrophy) (Tosun et al., Alzheimer's Dement. 18: 1370, 2022).
View Article and Find Full Text PDFBackground: Participant retention is a key determinant for a successful clinical trial. In Alzheimer's disease (AD) trials, participants are typically required to enroll with a study partner, which adds barriers to retention. Previous analyses of North American trial data found that most study partners were spouses and that such dyads had higher study completion rates than other study partner types.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Department of Neurology, Mayo Clinic, Rochester, MN, USA.
Background: Alzheimer's disease (AD) is an age-dependent neurodegenerative disorder with limited treatment options. As it progresses, synapse degeneration is the most important feature contributing to cognitive dysfunction. Mitochondria supply synapses with ATP for neurotransmitter release and vesicle recycling and buffer calcium concentrations.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!