Stroke and Alzheimer’s Disease

Mini Review

Phys Med Rehabil Int. 2016; 3(4): 1092.

Stroke and Alzheimer’s Disease

Ikramuddin F*

Department of Physical Medicine and Rehabilitation, University of Minnesota, 420 Delaware St, Minneapolis MN 55455, USA

*Corresponding author: Farha Ikramuddin, Department of Physical Medicine and Rehabilitation, University of Minnesota, 420 Delaware St, Minneapolis MN 55455, USA

Received: June 20, 2016; Accepted: July 18, 2016; Published: July 20, 2016


Stroke primarily affects the population over the age of 65 years, each year 795,000 people will experience new or recurrent stroke. It the most common cause of severe long-term disability (AHA 2010) in the US. Alzheimer’s disease (AD) is the most common form of dementia in the elderly. The prevalence of Alzheimer’s disease is known to increase as the population ages. Stroke and AD can occur together and result in deficits that appear to multiply. They share common vascular risk factors such as Hypertension, abdominal obesity and physical inactivity. It is difficult to differentiate the cognitive deficits that result from stroke and from Alzheimer’s disease individually and prognosticate function. The dysfunction and mismatch between the needs of the neural tissue to the mechanisms that regulate cerebral blood flow (CBF) have been postulated to result in cognitive deficits in both these disease processes. The neurovascular pathways are believed to be common to both the diseases and elucidate the potentiating effects that these two entities have on each other. This paper attempts to provide an understanding of the neurological pathways that may be common to the disease processes and pathology. Understanding of the mechanism of AD and cognitive deficits following stroke will help establish guideline and strategies in the prevention of these two diseases with similar and common neurological pathways.

Keywords: Stroke; Alzheimer’s disease; Hypertension; Cognitive deficits


Stroke is the leading cause of severe long-term disability in United States and fifth leading cause of death according to the data from National Vital Statistics System, 2015. Although there has been a decline in the death rate from stroke in the last 50 years, it is not clear if these changes result from a decrease in the incidence or reduced case fatality rates [1-3].

While the age standardized rates of stroke mortality have declined in the world during the last two decades, the prevalence of stroke, overall global burden of stroke has increased with most remarkable increase in the population aged 75 and above. Additionally, with the aging population in US, based on the 2010 age distribution, the forecasted stroke incidence is expected to rise in the next 40 years by 2.25 times [4]. This increase in the incidence of stroke events is expected to be specifically in the white population as well as Hispanic population.

The epidemiology of AD is notable for AD being the 6th leading cause of death, and fifth leading cause in those over the age of 65 years (Alzheimer Association, 2015). AD affects 5.4 million Americans. The incidence of Alzheimer’s dementia dramatically increases after the age of 65 from 53 new cases per 1000 people aged 65-74 to 170 per 1000 people aged 75 to 84; 231 per 1000 people older than 85. It is the only one of the top ten diseases in US that does not have prevention, cure or clear guidelines to slow its progression. Based on an economic model created by an independent research firm, a report from the Alzheimer’s Association projects that Medicare spending on people with Alzheimer’s disease will more than quadruple in just over a generation to $589 billion annually in 2050.

It is clear that both stroke and AD affect similar patient populations within an age range. However, the effect of AD on a patient with premorbid stroke is not clears. Conversely, the studies that evaluate the effect of stroke in a patient with pre-existing AD are conflicting. Nevertheless, cognitive deficits are an important prognostic indicator to the ability of patients to be discharged home safely, particularly in this age range. The ability of a clinician to prognosticate the recovery of stroke while considering the cognition at baseline and eventual support needed to prevent institutionalization cannot be over stressed in this patient population.

Many studies have hypothesized the cause of AD, which remains unclear. The pathological characteristic of AD consisting of neurofibrillary tangles; tau protein deposits as well as acetylcholine diminution along with calcium dysfunction associated with reactive astrocytosis leading to inflammation may be enhanced in the presence of atherosclerotic disease. Roher et al have repeatedly found strong correlation between large vessel atherosclerotic disease and neurotic plagues [5].

In AD, mitochondrial dysfunction is an important factor in the formation of AD, through the Oxygen Reactive Species ROS. Increased and unregulated inflammatory free radicals accumulate in AD, which promote neuronal apoptosis at vulnerable regions such as the hippocampus and amygdala. In mild and moderate AD, there is diminution of choline acetyl transferase activity. There is in mild and moderate AD, diminution of choline acetyl transferase activity is also noted. Choline acetyl transferase is responsible for the synthesis of the neurotransmitter acetylcholine. This results in loss of acetylcholine, specifically in areas of the brain associated with memory and learning. However, the cholinergic dysfunction is not considered to be the cause of the illness, but rather a consequence. This mechanism of decreased cholinergic activity is the target of the currently approved treatments for AD.

Citation: Ikramuddin F. Stroke and Alzheimer’s Disease. Phys Med Rehabil Int. 2016; 3(4): 1092. ISSN : 2471-0377