Lecanemab's apparent effectiveness follows years of disillusionment with earlier, comparable medications that were meant to delay or stop the course Alzheimer's disease. It contains monoclonal antibodies created in laboratories goal purging brain a material called as beta-amyloid, exactly like lot those other medicines. People disease tend have an accumulation beta-amyloid their brains, which l...

The beta-amyloid (Abeta) peptide is a principal component of insoluble amyloid plaques that are characteristic neuropathological features of Alzheimer disease (AD). The amyloid peptide also exists as a normal soluble protein that undergoes a pathogenic transition to an aggregated, fibrous form. This transition can be affected by extraneous proteinaceous elements and nonproteinaceous elements su...

Automated detection of amyloid plaques (AP) in post mortem brain sections of patients with Alzheimer disease (AD) or in mouse models of the disease is a major issue to improve quantitative, standardized and accurate assessment of neuropathological lesions as well as of their modulation by treatment. We propose a new segmentation method to automatically detect amyloid plaques in Congo Red staine...

Alzheimer disease (AD) involves glial inflammation associated with amyloid plaques. The role of the microglial cells in the AD brain is controversial, as it remains unclear if the microglia form the amyloid fibrils of plaques or react to them in a macrophage-phagocytic role. Also, it is not known why microglia are preferentially associated with some amyloid plaque types. This review will provid...

Minocycline is a second-generation tetracycline that effectively crosses the blood-brain barrier. It has remarkable neuroprotective qualities in models of cerebral ischaemia, traumatic brain injury, Huntington’s and Parkinson’s diseases. However, there is no evidence about neuroprotective effects of minocycline on AD. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized neurop...

Minocycline is a second-generation tetracycline that effectively crosses the blood-brain barrier. It has remarkable neuroprotective qualities in models of cerebral ischaemia, traumatic brain injury, Huntington’s and Parkinson’s diseases. However, there is no evidence about neuroprotective effects of minocycline on AD. Alzheimer’s disease (AD) is a neurodegenerative disorder characterized neurop...

Autosomal dominant forms of familial Alzheimer's disease (FAD) are associated with increased production of the amyloid beta peptide, Abeta42, which is derived from the amyloid protein precursor (APP). In FAD, as well as in sporadic forms of the illness, Abeta peptides accumulate abnormally in the brain in the form of amyloid plaques. Here, we show that overexpression of FAD(717V-->F)-mutant hum...

Overexpression of mutated human amyloid precursor protein (hAPP717V-->F) under control of platelet-derived growth factor promoter (PDAPP minigene) in transgenic (tg) mice results in neurodegenerative changes similar to Alzheimer's disease (AD). To clarify the pathology of these mice, we studied images derived from laser scanning confocal and electron microscopy and performed comparisons between...

Both the early and late-onset Alzheimer's disease affect millions of people throughout the world. A number of molecules have been implicated in the pathogenesis of Alzheimer's disease. These include presenilin 1 and 2 (PS1 and PS2), a beta-amyloid peptide, and tau protein. Presenilin 1 and 2 genes implicated in the early-onset familial Alzheimer's disease have been cloned. Both PS1 and PS2 are ...

Transgenic (Tg) mouse models overexpressing amyloid precursor protein (APP) develop senile plaques similar to those found in Alzheimer's disease in an age-dependent manner. Recent reports demonstrated that immunotherapy is effective at preventing or removing amyloid-beta deposits in the mouse models. To characterize the mechanisms involved in clearance, we used antibodies of either IgG1 (10d5) ...