Abstract
Alzheimer’s disease (AD) is the most common form of dementia, with a prevalence that increases with age. By 2050, the worldwide number of patients with AD is projected to reach more than 140 million. The prominent signs of AD are progressive memory loss, accompanied by a gradual decline in cognitive function and premature death. AD is the clinical manifestation of altered proteostasis. The initiating step of altered proteostasis in most AD patients is not known. The progression of AD is accelerated by several chronic disorders, among which the contribution of diabetes to AD is well understood at the cell biology level. The pathological mechanisms of AD and diabetes interact and tend to reinforce each other, thus accelerating cognitive impairment. At present, only symptomatic interventions are available for treating AD. To optimise symptomatic treatment, a personalised therapy approach has been suggested. Intranasal insulin administration seems to open the possibility for a safe, and at least in the short term, effective symptomatic intervention that delays loss of cognition in AD patients. This review summarizes the interactions of AD and diabetes from the cell biology to the patient level and the clinical results of intranasal insulin treatment of cognitive decline in AD.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia, with a prevalence that increases with age
AD is the most common form of dementia, with a prevalence that increases with age from 3% in people aged 65–74 to about 50% in people aged 85 or older
(40) is a competitive inhibitor of insulin binding to the insulin receptor (IR), and increased levels of this amyloid β (Aβ) could contribute to impaired insulin signalling and cognitive impairment in patients with AD
Summary
The increase in life expectancy in the developed world is accompanied with an increased number of patients suffering from two age-related diseases, Alzheimer’s disease (AD) and diabetes mellitus. Studies of patients with AD, and of AD animal models, have linked AβO with synaptic dysfunction, cognitive decline, inhibition of hippocampal long-term potentiation (LTP) component in memory, and learning and memory impairment [37,38,39,40,41,42,43,44,45,46] In these studies, AβOs were better correlated with dementia and synaptic loss Aβ in extracellular amyloid plaques [37,38]; toxicity mechanisms of amyloid and AβOs were reported to be similar [47,48,49]. The pathological mechanisms of AD and diabetes interact and tend to reinforce each other at the level of reduced cerebral blood flow and altered glucose metabolism, impaired insulin signalling, mitochondrial dysfunction, oxidative stress, advanced glycation end products, altered cholesterol metabolism, inflammation and cognitive impairment [3,5,6,7,16,76]
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