Alzheimer’s Disease (AD) is the most common form of dementia, a neurodegenerative disorder which makes a person lose his cognitive abilities slowly but steadily, altering his daily functioning, leading to various levels of physical and emotional stress.
Detected most commonly beyond an age of 65 years, an early onset of the disease, between ages 30 and 60 is also a possibility in a number of conditions, family history and genetics being the most common cause.
AD begins with short term memory loss problems which later sum up to severe issues, including loss of the identity of the patient to himself as well as those near and dear him. The exact point where AD actually catches up with a person’s nervous system is difficult to diagnose, which presents the main challenge in its diagnosis, as old age normally takes a toll on a person’s memory gradually, even on a natural basis. This poses the greatest challenge in detection and diagnosis of AD, which makes treatment all-the-more difficult. This is probably the reason why a mere 3% of the diagnosed cases manage to have a survival period of a maximum span of 14 years.
Being a progressive disease, it moves from a pre-demential state to a condition of mild cognitive impairment, before proceeding towards severe cognitive damage. It is the transition of the early stages of AD which is often misjudged as normal side-effects of aging, and hence hinders the initiation of treatment process.
Pathologically speaking, two major causes of AD, as observed from brains scan reports, include the formation of senile plaques and neurofibrillary tangles. The tangles are nothing but hyperphosphorylated Tau proteins (abundant in the neurons of the central nervous system), which become defunct and cannot participate in stabilization of microtubules, which in turn become disintegrated within neurons and hence cannot conduct nerve impulses. The senile plaques are formed of deposits of a protein called Beta Amyloid (Aβ), which is enhanced due to mutations in genes responsible for its breakdown and metabolism, and decreased secretion of selective neurotransmitters (namely norepinephrine). It is the formation of a large number of plaques and tangles which adds to the neurotoxicity of the condition, making it worse.
AD initially affects the memory compartment of the brain which leads to cognitive impairment that gets severe with time, induces mood swings and behavioral changes and leads to more confusion. These changes are more severe than normal age-related processes and normally it is the family members of the patient who get an idea. A caregiver, often from the family itself, is assigned the task of providing support physically and emotionally, to overcome these changes, but more than often it becomes a sorry and daunting task as he is always at the receiving end of things.
Apart from getting psychologic help from the physician after getting to know about the patient’s family history and the sequence of events from family members and relatives, brain scans are necessary to support the diagnosis, along with assessment of the patient’s intellectual functioning. Biochemical tests to detect the levels of Tau and Beta-Amyloid proteins in the cerebrospinal fluid (CSF) are conducted to supplement the information derived upon, thus far. As far as medications are concerned, physicians rely mostly upon anti-depressants, beta blockers, neuroleptics, and cholinesterase inhibitors. Supportive therapy is given to reduce brain inflammation and treatment of symptoms. Practicing a healthy diet and a clean lifestyle also helps overcome the mental stress to some extent.
AD has been the topic of extensive research over the past 15 years and 90% of what we know about the disease is all courtesy this. As of 2012, as many as 1000 clinical trials have been undertaken in order to understand the pathophysiology of the condition and obtain targets for therapeutic intervention. Recently, as many as 10 proteins in blood have been recognized as possible markers for AD. This comes as good news for patients as the main challenge for AD lies in distinguishing age-related consequences from those pertaining to AD. Globally, AD has been the cause of great economical burden, with the health costs alone in 2011 being as high as $183 billion. In the USA, around 5.4 million people get affected each year, with an estimate of 12 to 16 million getting affected by 2050.
Data from several cohort studies suggests that the incidence (the total number of new cases per unit person time) for the number of cases of AD is as high as 5 to 8 out of every 10 to 15 cases of dementia, per 1000 person years. Increasing age is the primary risk factor for this, with the risk of getting AD doubling for every 5 years post crossing 65, after which the incidence shoots up to 3 to 69 cases per 1000 person years.
As far as prevalence (the total number of cases in the population in a given time period) of AD is concerned, it is highly prevalent in the industrialized countries. As per data from the year 2000, the USA recorded a prevalence of 1.6% for people aged between 65 to 74 years, 19% for ages between 75 to 84 years, 42% for years 85 and above, showing an increase with increasing age. The numbers are predicted to get worse in 2030 and still higher in 2050, when 11 to 16 million people are estimated to be affected by AD. It is also one of the leading causes of deaths in the USA, with the number of deaths increasing annually.
According to estimates from a 2006 study conducted by WHO, globally, around .17% to .89% (11.4 to 59.4 million people approximately) are affected by AD, with the numbers expected to double and quadruple themselves by 2030 and 2050 respectively.
Prevalence is on the higher side in the Asian countries as well. In Japan, Korea and China, AD is twice as common as vascular dementia, the figures in China being 64.6% for people above 50 years of age. India has a high prevalence of dementia (including AD and vascular dementia), whereas Nigeria has a low prevalence rate for the same.
Studies have shown that the strongest relationship between age and development of pathological features typical to AD is round about near the age of 75 years, and surprisingly not more than that. This implies that people nearing or aged at 75 years stand the strongest chance of developing AD. This is another proof of age dependent incidence of AD.
Women have been shown to be slightly more prone to developing Ad than males, but that might be because of their high life expectancy. As far as ethnicity is concerned, African Americans have a higher (almost double) prevalence of AD as compared to whites, (21.3% as compared 11.1% for whites).
The exact cause triggering AD is still a mystery among researchers. The condition is believed to be caused by a combination of environmental and genetic factors, which lead to a series of neuropathological and physiological changes, leading to dementia and finally AD.
Several risk factors which are believed to contribute to the development of AD, which include family history, old age, insulin resistance, genetic mutations and predispositions, vascular factors, mental stress, brain injury and trauma and the recently researched upon topic, sleep deprivation, among others.
- Genetics: Heredity plays an important part in development of AD in people with a family history of the same. It is an autosomal (non sex linked) dominant disorder, causing 0.1% of the cases of AD approximately, all cases being exclusively the early onset of the disease. This affects roughly 3 individuals in 2 or more generations, out of which 2 cases are those of first degree relatives. The main genes involved in this regard are the Amyloid Precursor Protein (APP) gene, present on chromosome 21, and Presenilin 1 and 2, present on chromosomes 14 and 1 respectively. They are responsible for excess accumulation of the Aβ protein, which lead to loss of synaptic function, neuronal death and cognitive impairment. As far as the late onset disease is concerned, (also known as familial or sporadic form of the disease), the APOE ε4 (Apolipoprotein E Epsilon 4) genotype, which is another autosomal codominant trait with 3 alleles, has been linked to almost 80% of the cases of AD in this category. People with hypertension and blood pressure issues are at a higher risk of developing AD if they have this gene. Hypertension increases the amount of beta amyloid deposits in the brain, which leads to cognitive impairment. The highest risk of manifestation of the ill-effects of this gene is around the age of 70 years. Both APP and APOE ε4 contribute to the formation of Amyloid Derived Diffusible Ligands (ADDL) which bind to surface receptors on the neurons, and modify synaptic transmission, disrupting neuronal communication, eventually leading to dementia.
- Insulin Resistance: Insulin is the basic provider of glucose, which is needed by mitochondria to carry out metabolic activities and provide energy for cells to carry out their respective functions. This is no different for the cells (neurons) of the CNS, where there are ample insulin receptors, functioning with the energy derived from glucose metabolism. These insulin sensitive glucose receptors are located mostly in the medial and temporal lobes of the brain, which are related to normal functioning of human memory. Studies have shown the presence of insulin transporters in these regions which control the memory and learning departments, implying the contribution of insulin and glucose metabolism on the cognitive abilities of man. Moreover, insulin has also been shown to alter the deposition and accumulation of beta amyloid (Aβ), accelerate its intracellular trafficking, (which consequently reduces its extracellular accumulation). It is based on these observations, that has made researchers conclude that improved uptake of insulin in patients with AD could be a therapeutic measure against the disease. Positron emission tomography (PET) could be used to detect brain insulin and cerebral glucose metabolism rates, which are early markers for Alzheimer’s.
- Head injury and trauma: People, who sustain brain injuries and trauma, are always at an elevated risk of developing dementia in later stages of life. Older adults with a history of moderate traumatic brain injuries have been shown to be at 2.3 times the risk of developing AD or any other form of dementia, as compared to normal seniors with no such histories. For cases of severe trauma, this risk factor increases to 4.5 times that of a normal elderly person. Studies have also shown that these injuries lead to an imbalance in the amounts of Tau and beta amyloid proteins, which lead to AD as well. Increased risk of developing AD has been observed in patients with the APOE E4 genotype who have had a history of brain injury and trauma, though the exact link between these two is yet to be established.
- Depression has also been proven to be one of the potent risk factors in development of AD in the elderly. People refuse to indulge in activities they would normally enjoy, withdraw from all social attachments, have trouble thinking, remain isolated, are unusually emotional and tend to get agitated very easily. There have been statistically significant relationships between depression symptoms before the onset of AD in patients, according to previously published studies. Both depression and dementia affect the quality of life and impair the patient’s capability with old age. Though there is still confusion as to whether depression might coincide with the symptoms of AD, or whether it is a symptom spanning the gap between initial onset of the condition to complete manifestation of the disease, it is not incorrect to assume that people showing signs of depression, progressively worsening with time, are at a higher risk of developing AD in later stages of life.
- Infection: Chronic infection with microbes and parasites like different species of spirochetes, Treponemas sp. and herpes simplex virus type 1 have been proposed to enhance the risk of development of AD. This is mainly because, the beta amyloid protein, found in excess during this condition, also has anti-microbial properties. Moreover, these infections lead to neuronal disruption and dysfunction, which might lead to cognitive impairment and dementia.
- Epigenetics: Apart from the obvious genetic (hereditary) factors, environmental pressures also play a role in development of AD. Some of these epigenetic mechanisms which alter the heritable and non-heritable characters of an individual, include exposure to environmental stress, heavy metals, unhealthy diet and lifestyle practices, metabolic disorders which contribute to changes in phenotypes and properties of the genetic material, without undergoing a change in the gene sequence (eg: DNA methylation, chromatin remodeling, alterations in transcription mechanisms, histone modifications, RNA editing and interference among others). One of the major epigenetic factors seen to have posed serious threats on experimental laboratory animals is exposure to metals like lead and copper, which cause oxidative stress within the brains of these animals. Excess oxidative stress leads to alteration of methylation patterns in the neurons which lead to the formation of plaques as observed via brain scans and imaging techniques. Iron, released, as a result of breakdown and degradation of myelin sheaths in an aging brain, has also been observed as a potent risk factor. The repair process for these damaged myelin sheaths to restore homeostasis has also been concluded to be responsible for deposition of excess Tau and Beta-Amyloid deposits in the brain. Some studies suggest the role of air pollution in the development of AD as well.
- Vascular Factors: Vascular conditions (strokes and cardiovascular and cerebrovascular problems) have been concluded to play a crucial role in intensifying AD in the aging human brain. One logical connection to this might be the obstruction to cerebral blood flow because of these conditions, which induces malfunctioning of neurons and might also lead to their degeneration. Midlife is the peak age where these conditions have the strongest association with the possibility of an onset for AD, as compared to late adulthood, according to studies.
- Obesity: Deviation from a healthy lifestyle and physical activity has also been linked to AD by scientists and researchers. It has been seen that as the body gains more weight than normal, it becomes more resistant to lowering of blood-sugar levels by insulin, which is why the body keeps producing more insulin. This has even been linked to development of type 2 diabetes in a later stage of life, with the constant production of insulin. High levels of insulin cause inflammation in the brain and subsequently increase the levels of beta amyloid in the brain which eventually leads to AD.
AD affects three pathways which help in proper cognitive functioning in the human brain, communication between neurons interrupting synaptic signals, metabolism of nutrients and hampering the amount of energy needed for them to function properly, and repair of these damaged neurons and nerve fibers, which makes restoring normal conditions difficult and hence leads to progressive damage.
The neuropathological aspect of AD lies in the formation of senile plaques and neurofibrillary tangles in the brain, which causes neurotoxicity leading to loss of communication between neurons and synapses, mostly in the temporal and parietal lobes and medial parts of the cerebral cortex and hippocampus (the main part of the brain responsible for memory). However, it is to be remembered that the mere presence of these tangles and plaques do not guarantee a person’s susceptibility to developing AD. These should be present in large numbers and be in accordance to the other diagnostic criteria to distinguish between a normal aging person and an Alzheimer’s patient.
The tau protein is destined to phosphorylate and stabilize the microtubules forming the neurons, the former being responsible for providing the neurons with nutrients and energy. But during AD, the tau protein becomes chemically altered, leading to hyperphosphorylation of the same, becoming entangled with each other, hence interrupting the nutrient and energy supply of neurons via the microtubules, which themselves degenerate. This leads to formation of neurofibrillary tangles and degeneration of neuronal transport system. With the progressive worsening of the condition, these tangles accumulate in other parts of the brain including other cortical regions, high-order association regions, and at times the regions with sensory and motor neurons. (It can be noted that it is the chemical modification of the tau protein which leads to such a situation making a subject prone to AD. In case of mutations in the gene encoding for tau, there have been reported cases of frontotemporal dementia.)
On the other hand, the senile plaques are deposits of the beta amyloid (Aβ) protein, which is a small (39-43 amino acids long) segment, from its parent protein, amyloid precursor protein (APP), transcribed by the APP gene. This APP is necessary for the growth, development and damage repair of nerve fibers (neurons). AD causes the APP to transcribe in a faulty manner and fragment into smaller than usual parts, namely beta amyloid, which causes a disturbance in the calcium ion balance in nerve cells and induces their pre-matured death (apoptosis). Moreover beta amyloid deposits make their way within the mitochondria of nerve cells, hampering their metabolic processes, mainly insulin uptake and glucose metabolism which makes the cells prone to degradation.
Over the years there has been a debate on the exact pathologic effect exerted by plaques and tangles on AD in humans, with strong proofs coming in favor of abnormal amyloid metabolism and deposition of amyloid plaques. An example of beta amyloid being a sure trigger for Alzheimer’s comes from the fact that patients with Down’s Syndrome (trisomy of chromosome 21) often most exclusively tend to have an early onset AD within the age of 40. This becomes more evident because the APP gene, responsible for production of beta amyloid is also located on the same chromosome, along with an extra copy of it on the third set. This provides the scope of secretion of larger amounts of Aβ which exert their neurotoxicity and reduce the time normally taken for late onset AD to develop. Also, mutations in the APP gene have also been studied to contribute to greater deposits of Aβ. Added to that, the APOE ε4 serves as a severe risk factor, aiding in increased Aβ secretion, inability to clear the amount of Aβ produced around the neurons and so forth.
On the other hand, several reports have shown the absence of plaques in the brains of AD patients but their presence in the brains of normally aging people. A better link has been established, directly correlating the severity of Ad with the amount of neurofibrillar tangles formed in the brain as a result of faulty processing of the tau proteins. Destabilized microtubules lead to the formation of abnormal neural projections and hampers neuronal transport of signals, and increase production of Aβ as well.
Accessory mechanisms which pave the way for cognitive impairment and dementia include reduced activity of the synthetic enzyme choline acetyltransferase (CAT) and the catabolic enzyme acetylcholinesterase. This leads to a reduction in the synthesis of the neurotransmitter Acetylcholine, which hampers reaction time performance and cognitive functions, as obtained from biopsy reports of AD patients.
Oxidative stress and free radical production, which is a noted risk factor for most neurodegenerative disorders like Parkinson’s Disease and Amyotropic Lateral Sclerosis, has also been postulated as a risk factor in AD. Biopsies of brain tissues affected with AD have shown signs of oxidative damage, and plaques and tangles respond positively to antioxidant therapy, which point towards the effects of oxidative stress on the same. Release of reactive oxygen species (ROS) leads to impairment of homeostasis that exists between ion channels on cell membranes, the most profound effect being those on the calcium ion gates. Increased influx of calcium in the neurons leads to damage in DNA, protein synthesis, leads to untimely cell death (apoptosis) and affects amyloid protein metabolism and phosphorylation of tau proteins.
Inflammatory mechanisms play a vital role in any disease and in case of AD, it is no different. Increased levels of cytokines are seen in serum, cortical spaces with plaques and tangles and in the neurons. Transforming growth factor beta 1 (TGF-β1) has been seen to promote deposition of beta amyloid. Beta amyloid binds to several membrane receptors to induce neurotoxicity, out of which the receptor for advanced glycation end products (RAGE) has been studied to be involved in initiation of major immune responses. It mediates interaction between neuroglia (responsible for maintaining homeostasis among neurons) and Aβ, which activates the classical complement pathway via chemotactic and haptotactic movements.
Another plasma protein, clusterin, has been found to be another important contributor to the pathogenesis of AD, participating in the atrophy of the cortical regions related to cognitive stability in otherwise healthy individuals.
Normally AD is diagnosed on the basis of a person’s history, his family background, and moreover, observations made by the family members as to how and when the patient started showing signs of possible cognitive impairment and dementia. The most common sign of an AD patient is progressively subtle memory loss, which gradually gets associated with behavioral changes, mood swings, irritation and outbursts, finally marked by severe cognitive impairment, along with language and speech problems, loss of sense of time and place and visuospatial impairment.
Normally, a patient diagnosed with Alzheimer’s, passes through a number of stages. They can be summarized as:
- Pre-dementia / Pre-clinical phase: This phase begins in the cortical region just near to the hippocampus (entorhinal cortex, located in the medial temporal lobe, responsible for memory and navigation) and proceeds to the hippocampus with time. When tested neurophysiologically , this phase can be differentiated temporally as eight to ten (at times extending up to twenty) years before the actual onset of Alzheimer’s. This phase is termed as the phase of mild cognitive impairment (MCI) and is often mistaken for the natural effects of aging. This phase is typically marked by short term loss of memory and confusion regarding complex daily activities, recently learned facts, progressive problems with remembering, reasoning, problem solving and analyzing abilities and semantics. Often physicians term this phase as a clinical transitional period between normal aging of the brain and AD. No major problems are faced in this phase, however, and no tendency of suicide, or mood swings are noted in the subject.
- Early / Mild phase: This is the phase where impairment of cognitive functions continues to get severe than the previous phase, with difficulty to pursue daily routine activities, confusion with places, money (calculations), speech, problem with language, decreased vocabulary and difficulties in fluency of the same, difficulty with perceiving things, difficulty in co-ordination while carrying out fine motor tasks like writing, drawing, dressing (a stage called apraxia). These changes appear gradually, and the person is still able to perform these tasks on his own, but may need assistance once in a while. During this phase, the accumulation of plaques and tangles start taking place in the areas of the brain responsible for reasoning, memory and language, and brain scans show mild shrinkage of the cortex and hippocampus. This is the phase when the clinical diagnosis of AD is actually made. A patient and his family should seek diagnostic help during this time mostly, even when there is the least bit of doubt regarding his or her cognitive or reasoning skills.
- Moderate Phase: This is the next phase of severity where the patient slowly starts to lose the ability to perform all routine tasks on his own and seeks assistance most of the times. Inability to recall from memory, further shrinking vocabulary, complex motor sequences becoming all the more difficult to execute (increasing problems with numbers, progressively losing the ability to read, write, think logically, etc.). Moreover, this is the phase where behavioral and emotional irregularities and stresses start surfacing. A sense of irritation, restlessness, fear, anxiety, agitation and loss of impulsive control, especially during evening or nighttime are also common. Hallucinations and illusionary imaginations are also common in this phase for some patients. Urinary incontinence might develop in some patients as well. The patient might even refuse to recognize people near and dear to him, family members or relatives. Fear of his surroundings might force him to remain agitated and secluded from his own environment. All of these are as a result of spread of the plaques and tangles to areas of the cerebral cortex which control behavioral patterns, language, sensory processing and thought. It is important for a caregiver to stay as close to the patient as possible, and ensure his well being despite the emotional outbursts that the latter might have.
- Severe Phase: As suggested by the name, this is the most severe phase of the disease where the patient is totally dependent upon the caregiver. The patient cannot speak in proper sentences, only an off phrase or a word, sometimes suffering from complete loss of speech, though he might understand emotional signals directed at him. A sense of apathy prevails, without any emotional expression in any way. The patient cannot recognize his friends or family members in any way. Some of the other side-effects of this condition include weight loss, constant grumping or moaning noises, total loss of bladder and bowel control and an increase in the sleeping time for patients, as they do not wish to do anything else but remain in their own state. Pathologically this phase is denoted by a maximum atrophy of the cerebral cortex and hippocampus, with increased and widespread plaques and tangles. This is a period of terminal illness for the patient and is more than often followed by death, mostly due to other co-morbidities like diabetes, aspiration pneumonia or severe infectious diseases.
A thorough physical examination of the patient needs to be done, with special attention to testing the mental status of the patient. Several neuropsychological tests are available for this, including the Mini-Mental Status Examination (MMSE), Montreal Cognitive Assessment (MoCA) and the Saint Louis University Mental Status (SLUMS), out of which MMSE is said to have a low sensitivity and specificity. The patient is checked for his competency in concentration, carrying out special motor tasks on his own, ability to remember things, language and communication, perception, executive and visuospatial functions. However, these standard testing method only form a baseline in diagnosis and detection of AD, and stress more on confirming whether a patient is suffering from dementia or not.
To specifically check whether a patient has AD or not, a differential diagnosis needs to performed to substantiate and support the findings thus far, and zero in on Alzheimer’s, before going through the standard confirmatory guidelines. Common conditions weighed against, when testing for AD include, Aphasia, Parkinson’s Disease, Vascular Dementia, Dementia of the Frontotemporal lobe and that with Lewy Bodies, Huntington Disease Dementia, Chronic Traumatic Encephalopathy and Wilson’s Disease among others.
Clinical guidelines for the diagnosis of AD have been formulated by the National Institutes of Health-Alzheimer’s Disease and Related Disorders Association (NIH-ADRDA); the American Psychiatric Association, in the Diagnostic and Statistical Manual of Mental Disorders, Fourth Revision, Text Revision (DSM-IV-TR); and the Consortium to Establish a Registry in Alzheimer’s Disease (CERAD).
The DSM-IV-TR criteria for detection of ‘Dementia of the Alzheimer Type’ can be summarized as follows,
- The development of multiple cognitive deficits manifested by both of the following:
- Memory impairment (impaired ability to learn new information or to recall previously learned information)
- One or more other cognitive disturbances: aphasia (language disturbance), apraxia (impaired ability to carry out motor activities despite intact motor function), agnosia (failure to recognize or identify objects despite intact sensory function), disturbance of executive functioning
B. The cognitive deficits must each cause a significant impairment in social or occupational function and represent a significant decline from a previous level of functioning.
C. The course of disease is characterized by gradual onset and continuing decline.
D. The cognitive deficits are not due to any of the following:
- Other central nervous system conditions that cause progressive deficits in memory and cognition
- Systemic conditions that are known to cause dementia
- Substance-induced conditions
E. The deficits do not occur exclusively during the course of a delirium.
F. The disturbance is not better accounted for by another DSM-IV Axis I disorder (ie, a clinical disorder).
Clinical laboratory testing can also be used to support the findings from the criteria based neuropsychologic testing methods. These include blood tests to check for vitamin deficiency, nutritional content, liver enzyme levels and thyroid hormone levels to rule out any conditions related to their deficiencies.
Imaging techniques like Magnetic Resonance Testing (MRI) and Computed Tomography scanning (CT scans) can be useful in determining early phases of AD provided testing is done at the right time. Brain imaging and scanning techniques like Positron Emission Tomography, using a suitable imaging agent to view the plaques and tangles (eg: florbetapir F 18, flutemetamol F18,etc.) are the most reliable techniques to screen and detect signs of AD in patients. Electroencephalography (EEG) is referred to only in case of distinguishing against particular conditions, like prion related diseases. A lumbar puncture can be done in a few cases to determine the CSF levels of Tau and Aβ proteins.
As far as treating Alzheimer’s Disease is concerned, there are only symptomatic treatments available till date as scientists continue to dig deep into the mysteries of this neurodegenerative disorder to formulate possible therapeutic agents.
The use of cholinesterase inhibitors (ChEIs: Donepezil, Rivastigmine, Galantamine) and partial N-methyl-D-aspartate (NMDA) antagonists, modulators of increased synthesis of neurotransmitters like Acetylcholine or Glutamate can be used to slow down the process of cognitive impairment. Used mostly to treat the condition in its early stages, ChEIs have been found to be useful in treating the advanced form of the disease as well. However pulmonary and hepatic toxicity issues have been reported in patients with co-morbidities, hence a thorough knowledge of the patient’s health issues must be kept in mind. On the other hand, NMDA have been used successfully to lower the calcium ion influx and hence restore protein synthesis and processing in the brain. The most common NMDA used is memantine (Namenda, Namenda XR), an FDA approved drug, which can be used in combination with ChEIs to treat the advanced stages of the disease.
Major classes of medications to act on behavioral instabilities in advanced stages of the disease include anti-depressants, anxiolytics, beta-blockers, neuroepileptic and antiepileptic drugs and beta-blockers. However, these are only accessory medications with limited efficiencies.
Supportive nutritional and psychotic help is provided by the caregiver, who plays a vital role in keeping up with the emotional outbursts of the patient. A healthy and disciplined lifestyle is always necessary to keep up with any condition, and Alzheimer’s is no exception. Regular visits to the physician are necessary to keep a check on the progress of improvement in condition.
Research carried out these days focus mostly on the pathologic and biochemical pathways which are thought to be affected during AD, and one can only hope for a sure-shot therapeutic intervention, soon to be formulated, to cope up with this rapidly growing socio-economic health burden that is Alzheimer’s.