The relationship between general anesthesia and Alzheimers in elderly people is unclear.Little is known about the events that occur during and that actually cause Alzheimers disease. This is due to the fact that brain tissue from patients with the disease can only be studied after the persons death. However, it is known that one of the first aspects of the disease is a dysfunction in the gene that produces amyloid. Extracellular senile plaques (SPs), consisting of beta-amyloid (Aβ) peptides, and intracellular neurofibrillary tangles (NFTs) that are formed by hyperphosphorylated tau proteins, are two well-established pathological hallmarks of AD. Amyloid causes inflammation around the senile plaques of the brain, and too much build up of this inflammation leads to changes in the brain that cannot be controlled, leading to the symptoms of Alzheimers. Vascular
Vascular dementia accounts for at least 20% of dementia cases, making it the second most common type. It is caused by disease or injury affecting the blood supply to the brain, typically involving a series of mini-strokes. The symptoms of this dementia depend on where in the brain the strokes occurred and whether the blood vessels affected were large or small. Multiple injuries can cause progressive dementia over time, while a single injury located in an area critical for cognition such as the hippocampus, or thalamus, can lead to sudden cognitive decline. Elements of vascular dementia may be present in all other forms of dementia.Brain scans may show evidence of multiple strokes of different sizes in various locations.
In one study, classic oligodendrogliomas showed 1p loss in 35 of 42 (83%) cases, 19q loss in 28 of 39 (72%), and these were combined in 27 of 39 (69%) cases; there was no significant difference in 1p/19q loss of heterozygosity status between low-grade and anaplastic oligodendroglioma. 1p/19q co-deletion has been correlated with both chemosensitivity and improved prognosis in oligodendrogliomas. The gene products lost as a consequence of this codeletion may include mediators of resistance to genotoxic therapies. Alternatively, 1p/19q loss might be an early oncogenic lesion promoting the formation of glial neoplasms, which retain high sensitivity to genotoxic stress. Most larger cancer treatment centers routinely check for the deletion of 1p/19q as part of the pathology report for oligodendrogliomas. The status of the 1p/19q loci can be detected by FISH, loss of heterozygosity (LOH) analysis or virtual karyotyping. Virtual karyotyping has the advantage of assessing the entire genome in one assay, as well as the 1p/19q loci. This allows assessment of other key loci in glial tumors, such as EGFR and TP53 copy number status. Whereas the prognostic relevance of 1p and 19q deletions is well established for mixed oligoastrocytomas, the prognostic relevance of the deletions for low-grade gliomas is more controversial. In terms of low-grade gliomas, a recent study also suggests that 1p/19q co-deletion may be associated with a (1;19)(q10;p10) translocation which, like the combined 1p/19q deletion, is associated with superior overall survival and progression-free survival in low-grade glioma patients.