A randomized, controlled trial of a 3-month cognitive remediation program was examined for its efficacy at ameliorating deficits in social and emotion perception in 42 hospitalized patients with schizophrenia. Generalization of training effects to attention, memory, and executive functioning was also examined. The program included an eclectic mix of self-instruction, memory enhancement, inductive reasoning, and compensatory training procedures, while the control condition included participation in a leisure group that was matched to the experimental group for staff involvement time. Patient care management, including type and dose of antipsychotic medication, remained constant throughout the study period. The results indicated that the cognitive training program improved emotion perception, with some evidence of generalization to measures of executive functioning; other areas of neurocognitive functioning were largely unaffected. While cognitive training programs may improve targeted areas of neurocognitive processing, broad generalization effects to domains outside those targeted for intervention are not likely concomitants.
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http://dx.doi.org/10.1093/oxfordjournals.schbul.a006919 | DOI Listing |
Background: CT1812 is an experimental therapeutic sigma-2 receptor modulator in development for Alzheimer's disease (AD) and dementia with Lewy bodies. CT1812 reduces the affinity of Aβ oligomers to bind to neurons and exert synaptotoxic effects. This phase 2, multi-center, international, randomized, double-blind, placebo-controlled trial assessed safety, tolerability and effects of CT1812 on cognitive function in individuals with AD.
View Article and Find Full Text PDFAlzheimers 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
Imperial College London, London, United Kingdom; Division of Neurology, Department of Brain Sciences, Imperial College London, United Kingdom, London, London, United Kingdom.
Background: Liraglutide is a glucagon-like peptide-1 (GLP-1) analogue licensed for the treatment of type 2 diabetes mellitus (T2DM). Preclinical evidence in transgenic models of Alzheimer's disease suggests that liraglutide exerts neuroprotective effects by reducing amyloid oligomers, normalising synaptic plasticity and cerebral glucose uptake, and increasing the proliferation of neuronal progenitor cells.
Method: This is a multi-centre, randomised, double-blind, placebo-controlled, phase IIb trial of liraglutide in participants with mild to moderate Alzheimer's dementia, conducted at several centres in the UK.
Alzheimers Dement
December 2024
Innovation Center for Neurological Disorders, Xuanwu Hospital, Capital Medical University, Beijing, China;, Beijing, China.
Background: Individuals with type 2 diabetes mellitus (T2DM) face an increased risk of dementia. Recent discoveries indicate that SGLT2 inhibitors, a newer class of anti-diabetic medication, exhibit beneficial metabolic effects beyond glucose control, offering a potential avenue for mitigating the risk of Alzheimer's disease (AD). However, limited evidence exists regarding whether the use of SGLT2 inhibitors effectively reduces the risk of AD.
View Article and Find Full Text PDFBackground: Abnormal glucose metabolism in AD brains correlates with cognitive deficits. The glucose changes are consistent with brain thiamine (vitamin B1) deficiency. In animals, thiamine deficiency causes multiple AD-like changes including memory loss, neuron loss, brain inflammation, enhanced phosphorylation of tau, exaggerated plaque formation and elevated advanced glycation end products (AGE).
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