In this paper we review the hard-earned data, which present ischemic induction of amyloid precursor protein, presenilins, apolipoproteins and secretases genes, playing key roles in β-amyloid peptide generation. Presented data are strongly supporting a hypothesis that brain ischemia may be involved in the aetiology of sporadic Alzheimer's disease. Potential contribution and impact of ischemically activated genes on the development of sporadic Alzheimer's disease remain to be established at both genetic and functional levels. The identification of the genes involved in sporadic Alzheimer's disease induced by ischemia will enable to further define the events leading to Alzheimer's disease-related abnormalities. Additionally, knowledge gained from the reviewed studies should facilitate the elaboration of effective treatment and/or prevention of sporadic Alzheimer's disease.
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http://dx.doi.org/10.5114/fn.2012.32362 | DOI Listing |
J Prev Alzheimers Dis
February 2025
Department of Psychosomatic Medicine, University Medicine Rostock, Rostock, Germany; Deutsches Zentrum für Neurodegenerative Erkrankungen (DZNE), Greifswald, Rostock, Germany.
Background: Imaging studies showed early atrophy of the cholinergic basal forebrain in prodromal sporadic Alzheimer's disease and reduced posterior basal forebrain functional connectivity in amyloid positive individuals with subjective cognitive decline. Similar investigations in familial cases of Alzheimer's disease are still lacking.
Objectives: To test whether presenilin-1 E280A mutation carriers have reduced basal forebrain functional connectivity and whether this is linked to amyloid pathology.
Heliyon
January 2025
Laboratory of Neurochemistry and Behaviour, Experimental Neurobiology Unit, University of Antwerp, Belgium.
People with Down Syndrome (DS) are at high risk of developing Alzheimer's disease dementia (AD) and cerebral amyloid angiopathy, which is a critical factor contributing to dementia in sporadic AD. Predicting and monitoring the decline and onset of dementia is a diagnostic challenge and of essence in daily care and support for people with DS. In this literature scoping review, we first summarize the different blood-based biomarkers for AD in DS.
View Article and Find Full Text PDFJ Neuroinflammation
January 2025
Memory Unit, Neurology Department and Institut de Recerca Sant Pau, Hospital de la Santa Creu i Sant Pau, Universitat Autònoma de Barcelona, Sant Quintí 77-79, 08041, Barcelona, Spain.
Background: Neuroinflammation plays a major role in amyotrophic lateral sclerosis (ALS), and cumulative evidence suggests that systemic inflammation and the infiltration of immune cells into the brain contribute to this process. However, no study has investigated the role of peripheral blood immune cells in ALS pathophysiology using single-cell RNA sequencing (scRNAseq).
Methods: We aimed to characterize immune cells from blood and identify ALS-related immune alterations at single-cell resolution.
Curr Opin Psychiatry
January 2025
Centre for Healthy Brain Ageing, University of New South Wales.
Purpose Of Review: Recent advancements in molecular biomarkers and therapeutic options for Alzheimer's disease have brought into focus the need for greater progress in the second most common cause of dementia, vascular cognitive impairment and dementia (VCID). We examine how the study of monogenic causes of VCID has contributed to the understanding of its pathophysiology and potential biomarker and treatment research.
Recent Findings: It is widely accepted that conditions which disrupt the cerebral small vessels contribute to vascular pathologies including stroke and cerebral microbleeds, ultimately leading to vascular cognitive impairment and dementia.
Cureus
January 2025
Electrophysiology, 3Brain AG, Genova, ITA.
The natural product MGN-3 (Biobran) is a defatted, partially hydrolysed rice bran-derived hemicellulose enzymatically modified with an extract of . It has a high proportion of arabinoxylan. It has a protective action against intracerebroventricular streptozotocin-induced murine sporadic Alzheimer's disease and reverses spatial memory deficit in this disease model.
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