Endocannabinoids and Neurodegenerative Disorders: Parkinson`s
... acting on the eCB system may be due to the ability of these compounds to correct any potential dysregulation of eCB signals that might be instrumental in the pathogenesis of these disorders (Fagan and Campbell 2014). Indeed, far from being mutually exclusive, both types of responses may occur concom ...
... acting on the eCB system may be due to the ability of these compounds to correct any potential dysregulation of eCB signals that might be instrumental in the pathogenesis of these disorders (Fagan and Campbell 2014). Indeed, far from being mutually exclusive, both types of responses may occur concom ...
The Calcium Rationale in Aging and Alzheimer`s Disease
... controls did not. In two different clinical trials, it was shown that nimodipine has a beneficial effect, especially on functions involving learning, in patients with chronic cerebrovascular disorder or vascular dementia.9,10 These preclinical and clinical studies suggest that calcium channel blocke ...
... controls did not. In two different clinical trials, it was shown that nimodipine has a beneficial effect, especially on functions involving learning, in patients with chronic cerebrovascular disorder or vascular dementia.9,10 These preclinical and clinical studies suggest that calcium channel blocke ...
Galanin in Alzheimer s disease: Neuroinhibitory or neuroprotective?
... and entorhinal cortex concurrent with the appearance of dystrophic GAL-ir neurites in many of the plaques [60]. Occasional GAL-ir cell bodies were also observed in the hippocampus that were not evident in wild-type mice [60]. In addition, APP23 mice bearing two FAD-related APP mutations (V717I and K ...
... and entorhinal cortex concurrent with the appearance of dystrophic GAL-ir neurites in many of the plaques [60]. Occasional GAL-ir cell bodies were also observed in the hippocampus that were not evident in wild-type mice [60]. In addition, APP23 mice bearing two FAD-related APP mutations (V717I and K ...
Overexpression of mutant PrP induce amyloidogenesis in otherwise
... diseases called proteinopathies. The formation and spread of proteinaceous lesions within ...
... diseases called proteinopathies. The formation and spread of proteinaceous lesions within ...
Full Text
... severely affected, and white matter axonal spheroids were most frequent in areas adjacent to areas of severe white matter injury (Figure 5). The pattern of white matter involvement was similar in all case but varied based on disease duration (Table 1). In all cases frontal white matter was devastate ...
... severely affected, and white matter axonal spheroids were most frequent in areas adjacent to areas of severe white matter injury (Figure 5). The pattern of white matter involvement was similar in all case but varied based on disease duration (Table 1). In all cases frontal white matter was devastate ...
Alzheimer's disease
Alzheimer's disease (AD), also known as Alzheimer disease, or just Alzheimer's, accounts for 60% to 70% of cases of dementia. It is a chronic neurodegenerative disease that usually starts slowly and gets worse over time. The most common early symptom is difficulty in remembering recent events (short-term memory loss). As the disease advances, symptoms can include problems with language, disorientation (including easily getting lost), mood swings, loss of motivation, not managing self care, and behavioural issues. As a person's condition declines, they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Although the speed of progression can vary, the average life expectancy following diagnosis is three to nine years.The cause of Alzheimer's disease is poorly understood. About 70% of the risk is believed to be genetic with many genes usually involved. Other risk factors include a history of head injuries, depression, or hypertension. The disease process is associated with plaques and tangles in the brain. A probable diagnosis is based on the history of the illness and cognitive testing with medical imaging and blood tests to rule out other possible causes. Initial symptoms are often mistaken for normal ageing. Examination of brain tissue is needed for a definite diagnosis. Mental and physical exercise, and avoiding obesity may decrease the risk of AD. There are no medications or supplements that decrease risk.No treatments stop or reverse its progression, though some may temporarily improve symptoms. Affected people increasingly rely on others for assistance, often placing a burden on the caregiver; the pressures can include social, psychological, physical, and economic elements. Exercise programs are beneficial with respect to activities of daily living and can potentially improve outcomes. Treatment of behavioral problems or psychosis due to dementia with antipsychotics is common but not usually recommended due to there often being little benefit and an increased risk of early death.In 2010, there were between 21 and 35 million people worldwide with AD. It most often begins in people over 65 years of age, although 4% to 5% of cases are early-onset Alzheimer's which begin before this. It affects about 6% of people 65 years and older. In 2010, dementia resulted in about 486,000 deaths. It was first described by, and later named after, German psychiatrist and pathologist Alois Alzheimer in 1906. In developed countries, AD is one of the most financially costly diseases.