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Alzheimer's Disease FAQ
- What is Alzheimer’s disease?
Alzheimer’s disease (AD) is a brain disorder characterized
clinically by progressive cognitive declines in memory, language,
and other abilities. Physical changes within the brain include
the presence of ß-amyloid plaques, neurofibrillary tangles
(NFTs), and cell loss.
- What is the difference between Dementia and Alzheimer’s
disease?
Dementia is a general term describing an individual who has
experienced a decline in their cognitive abilities to the point
where they are unable to take care of themselves. There are
several possible causes for dementia. Alzheimer’s disease
is the most common cause of dementia in the elderly. Other causes
include vascular disease, Parkinson’s disease, and traumatic
brain injury.
- What are the earliest signs of Alzheimer’s disease?
Typically the earliest symptom is difficulty with memory, particularly
recalling events or facts recently learned. Long-term memories
such as childhood experiences are not impacted in the early
stages. Other early signs may include difficulty finding words
when speaking or directional confusion while driving. AD is
not the only cause of memory problems. Memory problems can result
from thyroid disease, vitamin deficiencies, or medication side
effects. Therefore it is important to talk to your doctor if
you or your loved one is experiencing changes in memory ability.
- Who is at risk for AD?
AD is primarily a disease of the aged. In fact the greatest
risk factor is age. It is currently estimated that close to
50% of adults over the age of 85 have some form of dementia
including AD. There is also a greater risk for AD associated
with a family history of the disorder. Also common variations
in some known genes, such as the APOE gene located on chromosome
19, influence risk for AD.
- Will I know that I have AD if I get tested for the
APOE gene?
The Apolipoprotein E (APOE) gene exists in three common forms
or alleles and the e4 allele is a known modifier of age of onset
for AD. APOE gene variations have been the most robust findings
in late onset AD. However, not all individuals with the e4 form
of APOE develop AD, therefore its use in diagnosis of AD has
not been validated.
- What is early onset AD?
Early-onset AD cases have an age of onset prior to 65, and usually
demonstrate a strong family history with an autosomal dominant
mode of inheritance which means the disease is seen in every
generation regardless of gender. Early-onset AD is primarily
caused by extremely rare genetic mutations in either the ß-amyloid
precursor protein gene (bAPP) or one of the presenilin genes
(PS-1 & PS-2). These cases are very rare, accounting for
less than 5% of all AD cases.
- What are the current treatments for AD?
Current treatment is aimed at slowing the disease progression.
At present there is no cure. Treatment includes medication that
helps increase certain brain chemicals affecting memory and
reducing secondary damage to the brain from inflammation. These
medications are Aricept (donepezil), Exelon (rivastigmine) Razadyne
(formerly named Reminyl) (galantamine), and Namenda (memantine).
Aricept, Exelon and Razadyne are cholinesterase inhibitors which
increase a neurotransmitter called acetylcholine in the brain.
This helps alleviate some of the symptoms of AD. However, the
principal mechanism of action of Namenda is believed to be the
blockade of current flow in the brain through channels of N-methyl-d-aspartate
(NMDA) and modulation of NMDA receptor activity can increase
or decrease excitability of brain circuits. Similar to cholinesterase
inhibitors, this also only provides some improvement of AD symptoms.
Other treatment includes education and support. Research has
shown that treatment works best if the disease is diagnosed
and treated early.
- Why have a free memory screen?
There are several causes for memory changes as we age including
AD, depression, medication side-effects, vitamin deficiencies,
etc., many of which are treatable, if not curable. Why wait
and wonder? Taking a quick 20-minute paper and pencil test can
allay your concerns and/or lead to the proper treatment. Screening
positive simply means further evaluation is needed.
- How is AD diagnosed?
AD is only diagnosed for certain after death via a brain autopsy.
However, a clinical diagnosis by specialists is often very accurate
and is best to ensure proper treatment. The clinical diagnosis
involves seeing a physician (typically a neurologist) who must
rule-out treatable causes of the cognitive changes. This is
done via laboratory work-up and a neurological examination.
A neuropsychological evaluation is also an important component
of the process and involves comprehensive testing of cognitive
abilities including memory, attention, language, higher order
mental functions and emotional status. The third component of
a dementia work-up is getting a picture of the brain (e.g.,
brain MRI or CT). Medicare and/or other insurances typically
cover the diagnostic work-up.
- Once diagnosed, what should I or my caregiver do?
Receiving a diagnosis of AD is difficult. It is the beginning
of a challenging road for both the patient and their loved ones.
Patients should try to stay as active as possible. Medications
are available that can slow down the disease progression. Participating
in clinical trials may also be an important option. Support
groups are often helpful for patients in the early stage and
for caregivers throughout the course of the illness (which lasts
on average about seven years). It may be necessary to seek the
advice of an elder law attorney for appropriate legal and health
care planning. Education regarding possible community resources
is also very important. Click
here for Resources for Caregivers.
- What is the cause of AD?
There are likely to be several causes of AD but most of the
research has focused on the Ab and tau proteins, which accumulate
in the brain of AD patients. These two proteins form two markers
for the disease called ß-amyloid plaques and neurofibrillary
tangles.
- What is Ab?
Ab (also known as ß-amyloid) is the protein which accumulates
in the brain of AD cases and is considered a hallmark of this
disease. As it accumulates, neurons are damaged leading to their
malfunction which subsequently manifests as memory loss and
other cognitive change. This process, once begun, is naturally
relentless but much evidence suggests that if Aß could
be prevented from accumulating the disease would be halted.
- What are neurofibrillary tangles (NFTs)?
NFTs are intracellular defects, involving the neurons and can
be seen in microscopic sections after staining. These appear
as spherical or flame shape objects depending on the location
within the brain. Molecular biological analyses show that the
NFTs are composed mainly of abnormally-phosphorylated tau protein.
- What is Tau?
Tau is one of the main components of NFT, a neuron-specific
protein that is the major constituent of neuronal microtubules.
- What else can be done?
Some patients opt to participate in research or clinical trials.
Research is not the same as treatment. Historically, research
has led to important discoveries that make our lives better
such as new drugs to treat serious illnesses like heart disease
or diabetes. Participating in a clinical trial may or may not
help you but it could help others in the future. We
offer numerous clinical trials that are focused on AD.
Also see:
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"Every patient with Alzheimer's Disease displays
the disease slightly differently, but the underlying disorder
exhibits common signs, symptoms and pathology. It is very helpful
for patients and caregivers to know what these are." -
Dr. Michael Mullan
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