Alzheimer’s Disease
Alzheimer’s disease (AD) is the most common form of dementia and is a neurodegenerative disease which mostly afflicts people above 65 years of age.
Statistics reveal that around 24 million people worldwide are suffering from dementia out of which about 60% dementia is due to Alzheimer’s disease. The clinical symptoms and signs of Alzheimer’s include progressive cognitive deterioration, along with inability to deal with daily activities as well as behavioral changes and various neuropsychiatric symptoms.
Alzheimer’s disease manifests itself in the form of amnesia; which is memory loss that begins as mild forgetfulness but gradually becoming greater as the illness progresses although the patient is able to preserve older memories safely.
It has been found that Plaques containing the misfolded peptides called amyloid beta (Aβ) start forming in the brain much before even before the clinical symptoms and signs of the Alzheimer’s disease are observed. The neurofibrillary tangles and amyloid plaques are the basic pathological signs of the Alzheimer’s disease.
The causal factors behind Alzheimer’s are not yet known. Studies reveal that genetic factors play an important role as shown by the dominant mutations in three different genes which are responsible in cases of early onset and familial cases of Alzheimer’s disease. The ApoE gene is held responsible for the commonly occurring late onset Alzheimer’s disease. These four genes may carry variants or mutations that lead to increased risk for the disease but they account for only 30% of the genetic picture of the Alzheimer’s. any mutations in either of these four genes can cause accumulation of Aβ in the brain is excessive amounts which is the main component of the senile plaques in brains of patients suffering from Alzheimer’s Disease.
Proper medication can limit and alleviate the symptoms and signs of the disease; however, they are unsuccessful in changing the course of the underlying pathology.
Further studies have tried to understand how the synapses are lost in Alzheimer’s Disease before the plaques and tangles develop as well as how synaptogenic compounds can help in treating the Alzheimer’s Disease. It has been pointed out that as previously believed the Alzheimer’s Disease is not primarily a disease of plaques and tangles; rather it is mainly a disease of synapses. Therefore, it is important to target the loss of synapses in the treatment of Alzheimer’s disease which will also eliminate other aspects of the disease such as the loss of neurons, A Beta, elevated levels of the toxic protein, the appearance of plaques, as well as loss of cognitive function.
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