The neural basis of visuospatial deficits in Alzheimer's disease is unclear. We wished to investigate the neural basis of visuospatial perception in patients with Alzheimer's disease compared with healthy elderly comparison subjects using functional magnetic resonance imaging (fMRI). Twelve patients with AD and thirteen elderly comparison subjects were investigated. The patients were recruited from the local clinic and comparison subjects were from spouses and community. All participants underwent fMRI whilst viewing visuospatial stimuli and structural MRI, and findings were analysed using voxel-based morphometry. The comparison group activated V5, superior parietal lobe, parieto-occipital cortex and premotor cortices. The AD group demonstrated hypoactivation in the above regions and instead showed greater activation in inferior parietal lobule and activated additional areas. There was no structural atrophy above and beyond that found globally in patients in the identified regions of BOLD activation. To our knowledge, this is the first study to explore the neuroanatomy of perception of depth and motion in Alzheimer's disease. These specific functional deficits in AD provide evidence for an underlying patho-physiological basis for the clinically important symptom of visuospatial disorientation in patients with AD.
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http://dx.doi.org/10.1016/j.pscychresns.2008.11.002 | DOI Listing |
Sci Adv
January 2025
Centre for Misfolding Diseases, Department of Chemistry, University of Cambridge, Cambridge CB2 1EW, UK.
Several human disorders, including Alzheimer's disease (AD), are characterized by the aberrant formation of amyloid fibrils. In many cases, the amyloid core is flanked by disordered regions, known as fuzzy coat. The structural properties of fuzzy coats, and their interactions with their environments, however, have not been fully described to date.
View Article and Find Full Text PDFSci Transl Med
January 2025
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder. Antiamyloid antibody treatments modestly slow disease progression in mild dementia due to AD. Emerging evidence shows that homeostatic dysregulation of the brain immune system, especially that orchestrated by microglia, plays an important role in disease onset and progression.
View Article and Find Full Text PDFChembiochem
January 2025
China Pharmaceutical University, Department of Pharmaceutical Science, #639 Longmian Dadao, Jiangning District, 211198, Nanjing, CHINA.
Alzheimer's disease (AD) is a significant neurodegenerative disorder primarily affecting individuals over the age of 65. It is characterized by impairments in memory, thinking, analytical judgment, visuospatial recognition, and mood. In recent years, the development of protein and peptide drugs targeting amyloid-beta (Aβ) has gained momentum, with several therapies entering clinical trials and even receiving marketing approval.
View Article and Find Full Text PDFStem Cells
January 2025
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX13QX, UK.
The large majority of Alzheimer's disease (AD) cases are sporadic with unknown genetic causes. In contrast, only a small percentage of AD cases are familial, with known genetic causes. Paradoxically, there are only few validated mouse models of sporadic AD but many of familial AD.
View Article and Find Full Text PDFBrain
January 2025
U1237, Physiopathology and Imaging of Neurological Disorders (PhIND), Neuropresage Team; INSERM, University of Caen Normandy; GIP Cyceron, 14000 Caen, France.
Curing Alzheimer's disease remains hampered by an incomplete understanding of its pathophysiology and progression. Exploring dysfunction in medial temporal lobe networks, particularly the anterior-temporal (AT) and posterior-medial (PM) systems, may provide key insights, as these networks exhibit functional connectivity alterations along the entire Alzheimer's continuum, potentially influencing disease propagation. However, the specific changes in each network and their clinical relevance across stages are not yet fully understood.
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