Scientists show how gene expression controls synaptic plasticity in the aging human brain
Scientific evidence shows how the cognitive decline in Alzheimer’s disease (AD) is caused by the buildup of amyloid beta proteins, which promote synaptic malfunction. One of the neuropathological features in the brains of patients with AD is the degeneration of the basal forebrain cholinergic neurons, leading to a decrease in the number of cholinergic projections to the hippocampus. As a symptomatic treatment of AD, cholinergic neurotransmission is enhanced by the use of certain drugs, known as acetylcholinesterase inhibitors. For better prevention and treatment of cognitive disorders like AD and schizophrenia, it is necessary to understand how acetylcholine regulates synaptic transmissions.
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