Neurological Disorders: Alzheimers
What is Alzheimers Disease (AD)?
Alzheimer's Disease or Alzheimers Dementia (AD) is the commonest cause for dementia and the incidence of this dementing illness increases with age.
Dementia is a neurological condition, and a Neurologist is frequently involved in the care of these patients. A dementing illness manifests with chronic mental (thinking or cognitive) deficits significant enough to affect somebody’s functioning of daily life. In the beginning it may be subtle, however as time passes it affects personal, family, social and occupational spheres of life and also gets noticed by others.
Who gets Alzheimers disease?
Majority of AD patients are above 60 years. Only 5 to 10% of patients develop this before 60 and when it happens it may be familial (hereditary). Most of the old age AD are sporadic (random and non familial).
It affects both sexes and all races. In the US blacks are affected more than whites. Almost all patients with Down’s syndrome will develop this disease if they survive around age 40 or so.
What is the pathology of AD?
Alzheimers dementia is a neurodegenerative type of disease and affected individuals lose more and more of their neurons (nerve cells) in a gradual manner. It affects the cerebral hemispheres diffusely, although the maximum damage is seen in the parieto temporal cortex. Parts of temporal lobe called medial temporal lobe including hippocampus etc are mainly concerned with storage and processing of memory and these regions are affected early & severely.
At the microscopic level there are certain characteristic findings seen with AD including;
- Neurofibrillary tangles
- Senile plaques
- Granulovacuolar degeneration
- Loss of neurons & synaptic dysfunction
A neurochemical called acetylcholine concentration decreases in certain areas of the brain in AD patients.
The vast majority of Alzheimers dementia (more than 90%) is non hereditary type. The hereditary forms characteristically present at an early age, and family history is frequently available. Some of the genetic mutations that have been identified so for include; presenilin 1, presenilin 2 & amyloid precursor protein.
How does patient present?
The typical cases of AD present with a gradual onset and progression. Initially symptoms are subtle and include short term memory loss. Remembering the names and numbers are difficult. As the disease progresses, language difficulties, apraxias, agnosias (see below) and severe memory loss typically dominate the clinical picture, and patients will have increasing difficulty in organizing daily. Later insight & judgment will be affected too, and patient will become more & more dependent on his family members or care givers.
Apraxia means an inability to perform previously learned motor activity despite having the physical ability & desire to perform it. Agnosia is a loss of a person’s ability to recognize things by using the special senses like vision, hearing, smell, taste etc while these senses themselves are intact.
At an advanced stage patients are frequently institutionalized and require total care. Terminally ill patients are generally mute, bed bound, and finally succumb to the disease due to infections, malnutrition, and immunosuppression etc.
Currently AD is diagnosed mainly based on clinical criteria however the diagnosis is more and more assisted by the laboratory findings too. Initially structural imaging studies of the brain like CT or MRI scan are arranged followed by functional imaging studies like SPECT scan and PET scan etc are arranged, especially the Amyloid PET scan (Florbetapir amyloid PET scan) provides an invaluable clue towards the presence of absence of AD by showing the presence or absence of amyloid deposition in the brain. CSF (cerebrospinal fluid) analysis is also gaining significant attention (CSF tets like phosphorylated tau, total tau, beta amyloid 1-42 peptide tests etc). Brain biopsy is the definitive test but rarely employed on routine basis due to the risks and cost involved with the procedure, also due to no curative treatment yet available for AD, and also because the recent availability of reliable amyloid PET scan and the CSF tests make the need for the brain biopsy less.
There are also certain genetic tests available for familial type of AD.
For Alzheimers no curative treatment is yet available. There are several medications available but help only on symptomatic basis e.g. donepezil (aricept), memantine (namenda) etc, these agents may help in keeping the dementia symptoms under bay but do not affect the progression of the AD.
Additional measures that may also help in slowing down the progression of AD along with some symptomatic improvement as well include proper dietary modifications (diet rich in vegetables/fruits, rich in legumes, nuts, low in saturated fat etc - generally called as Mediterranean diet), adequate daily physical exercise, adequate daily mental exercise (solving crossword puzzles, brain teasers etc), and increased socialization through referrals to senior community centers & day treatment programs etc.
One of the primary pathologies of AD is deposition of an abnormal protein product called as beta amyloid in and around the neurons (brain cells) and this deposition acts as a toxic material and contributes to the degeneration of the brain cells (neurons) resulting in dementia and there are lots of research activities going on to prevent or reduce the deposition of the toxic beta amyloid material in the brain, so far there is no major success however there is hopes that this type of therapeutic intervention will help the AD patients, not only help in the reduction of the symptoms but also there is hope that the onset of the AD itself may be preventable with these anti-beta amyloid agents (hopes of cure for AD is possible too).
As Alzheimers disease advances psychiatric & behavioral issues are also a major concern and at that moment judicious usage of psychiatric medications (antipsychotic, antidepressant, anti anxiety agents etc) along with supportive treatment for both the patient & family is of paramount significance.
Alzheimers to Neurology Articles
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