Decrease in cognition and memory is often not noticed by the caregivers of the person with AD at the onset of the condition. Decrease in behavior and mood accompanies cognitive impairment and is the main complaint noticed by caregivers. Other signs noticed are difficulty in feeding, urination, and bowel control difficulties. Neuropsychiatric features such as personality changes, and agitation and dementia may be present from the onset of the condition. Behavioral symptoms that occur after the onset of the disease, such as inappropriate speech and aggression, may be misinterpreted as the results of psychotic episodes and may result in a delayed diagnosis.
Alzheimer disease (AD) appears to be related to genetics and age, and a number of known risk factors including sex, environment, and health behaviors may also influence susceptibility. Most current knowledge, however, has centered on mutations in specific genes associated with familial AD and rare, monogenic forms of the disease. However, there also may be rare cases involving mutations in genes that are also known to have a significant impact on risk for normal aging or other diseases. More recently, however, it became apparent that a number of common genetic variants related to Alzheimer disease may actually increase risk for Alzheimer-associated diseases.
If current rates continue over the next 20 years, more than one million Americans are likely to have Alzheimer's disease. If current trends change, as anticipated by some, the projected number of Americans who have this disease will nearly double.
AD is a progressive disease marked by behavioral disorders, cognitive deficits, and a shortage of productive brain functioning. The most common type of AD is Alzheimer's disease. It has a prevalence of about 2% in the USA among people 65 and over. In nursing homes, about half the patients are AD patients with about the same number of female patients receiving AD treatments.
Even if our study shows good results in terms of a reduction of the cognitive decline, an effect has to be attributed to the therapy only. Even though we found positive effects on the activities of daily living, an effect on neuropsychiatric symptoms was not observed, which may be explained by methodological reasons.
Tasks that can improve the quality of life of people with AD are of great importance for them and can be targeted by health care providers when considering the type of treatment to offer.
In general, patients' knowledge and perceptions and patient-clinician relationships matter for the ability to motivate patients to enroll in clinical trials. Physicians and other clinicians should take a proactive approach to promoting enrollment of patients with cognitive impairment in clinical trials.
Each individual (n=9) was scanned four times with a total of four time-point scans and was examined pre- and post-incubation for changes in amyloid-β (Aβ) and tau (MAPT). Results indicate that 18F-MK-6240 did not produce reductions in Aβ levels. It was also not able to prevent the progression of tau hyperphosphorylation assessed as the increase in tau S262. Further work on the mechanisms of action and the potential utility of 18F-MK-6240 is ongoing. This paper is open access under the terms of the BioMed Central Open Access Policy.
[Alzheimer disease is caused by accumulation of amyloid beta () particles in the brain, primarily in the regions that process memory such as the hippocampus and portions of the cerebral cortex. For a long time, there have been two major theories for the exact origin of the amyloid particle. One theory was that it came from a protein that is normally produced in the nervous system, and the other was that the amyloid beta came from an organism that died elsewhere in the body, with the amyloid being spread via the nerve cells during their life cycles.
The latest literature shows that the majority of studies in this area are not relevant to our daily clinical practice. Our studies suggest a few ways by which more targeted research may be accomplished for primary or secondary prevention.
MK-6240 when given in combination with other drugs exhibited only low-level activity. However, MK-6240 activity could be significantly increased by the combination with AIs, tricyclic antidepressants or anxiolytics in a dose-response dependent manner. Results from a recent paper suggest that MK-6240 alone is not a promising compound for AD treatment or for improving cognitive performance in AD patients. However, further development of combinated MK-6192 is warranted, especially with AIs, tricyclic antidepressants or anxiolytics.