Alzheimer's disease is the most common type of dementia. It is a progressive disease beginning with mild memory loss and possibly leading to loss of the ability to carry on a conversation and respond to the environment.

1. Subject : Biology
Unit : 4
Alzheimer disease
Done By : Shamma Salem 11 E
Teacher : Zeinab Albishah

2. Introduction :
Alzheimer's disease is a neurological disorder that affects the
brain and causes problems with memory, thinking, and behavior.
It is the most common cause of dementia among older adults,
and the symptoms can start gradually and worsen over time. The
disease occurs when the brain cells degenerate and die, leading
to a loss of brain function. The exact cause of Alzheimer's disease
is still unknown, but factors such as age, genetics, and lifestyle
may play a role. Unfortunately, there is currently no cure for
Alzheimer's disease, but treatments can help manage symptoms
and improve the quality of life for those affected.

3. Alzheimer's patients may go through mood
swings, struggle to learn new things, and lose
track of their loved ones. Alzheimer's disease
causes numerous neurons in the brain to die,
causing tissue loss. A brain scan can
demonstrate that. According to some experts,
neurofibrillary tangles and amyloid plaques
are two protein complexes responsible for the
widespread cell loss. Neurofibrillary tangles,
which are made of tau protein, make it more
difficult for neurons in a sick brain to acquire
nutrition and communicate with one another.
Tau proteins build microtubules in a healthy
brain, which are cellular structures that carry
nutrients and support the cytoskeleton. Beta-
amyloid, a subset of the larger amyloid
precursor protein, is what makes up amyloid
plaques. Amyloid precursor proteins are used
to make beta-amyloid, which is then broken
down outside the cell. Apolipoprotein E, or
APOE, which helps break down, facilitates this
process.

4. Because beta-amyloid is chemically sticky it builds up, causing protein
aggregation and plaque development. These plaques cause cell death
and harm to neurons. The expression of the APOE4 gene increases the
chance of beta-amyloid aggregates, increasing the risk of developing
Alzheimer's disease, and is an example of a genetic risk factor. In
addition to genes, several elements can increase a person's risk of
developing Alzheimer's disease.
The prevalence of age-related brain alterations and pathological
changes, such as those seen in dementia and Alzheimer's disease, is
correlated with a notion termed reserve, which links life experiences
including exercise, food, and education. The term "brain reserve" refers
to the physiological traits of the brain, including its size and the number
of neurons and synapses. These physical characteristics can have an
impact on pathology. The brain's capacity to rewire itself and find
different methods to carry out a task in the event that the original
pathway is disrupted is known as cognitive reserve.

5. One who has a strong cognitive reserve is better
able to handle brain damage than one who has
a poor reserve. The idea of cognitive reserve has
been connected to levels of education and
employment based on epidemiological studies.
Higher levels of education and vocational
attainment are thought to be associated with
higher levels of cognitive reserve and lower
vulnerability to Alzheimer's disease.
Having a high cognitive reserve means that an
individual can manage brain damage better
compared to someone with a low cognitive
reserve. According to epidemiological studies,
cognitive reserve is connected to education and
job status. It is believed that people who have
received more education and have better jobs
are likely to have a higher cognitive reserve.
They have also shown to have less chance of
developing Alzheimer's disease.

6. Generally, people who come from low-income populations tend to have limited healthcare access
and are more inclined to adopt unhealthy lifestyle habits, such as smoking, unhealthy eating, and
physical inactivity. These lifestyle factors can contribute to the onset of chronic diseases like
Alzheimer's, fatness, and diabetes.
Despite making significant strides in research, there are still several unclear factors that can lead to
Alzheimer's disease. Some of these factors include questions about the impact of environmental
toxins such as metals and air pollution, the microbiome, and the immune system. Plenty of research
has been done to identify better ways to care for patients to lessen the impact that Alzheimer's
disease has on individuals and their families, while scientists try to understand the science behind
the disease and find a solution.

7. As living beings, we constantly take in information from our environment and process it. Signals
include things like light, heat, smells, touch, and sound. The cells in our bodies are constantly getting
messages from other cells. These signals are crucial for maintaining and promoting vital processes in
cells, such as cell division and differentiation. Signals are frequently chemicals that are present in the
extracellular fluid that envelops cells. These substances can originate in the body from a great
distance (endocrine signaling via hormones), close proximity (paracrine signaling), or even the exact
cell (autocrine signaling).
In addition to altering the
metabolism of the cell receiving
the signal, signaling molecules
can also affect how genes are
expressed (transcribed) inside
the nucleus of the cell, or even
both.
Description of Signal Transduction :

8. Overview of Cell Signaling :
Three steps can be identified in cell signaling :
1. Reception: An outside signaling molecule is picked up by a cell. A signal is recognized when a ligand,
a chemical signal, interacts to a receptor protein either within or on the surface of a cell.
2. Transduction: The receptor protein is altered in some way when the signaling molecule attaches to
it. The transduction process is started by this modification. Usually, there are numerous phases in the
process of signal transduction. The following molecule in the signal transduction cascade is altered by
each relay molecule.
3. Response : The signal finally causes a particular biological reaction.

9. A cellular response is triggered when membrane receptors contact the signal molecule (ligand) and
cause the production of a second signal (also known as a second messenger). This receptor changes
shape or associates with another protein to transmit information from the extracellular environment
to the interior of the cell when a particular ligand binds to it. Examples of membrane receptors
include receptor tyrosine kinases and G protein-coupled receptors.
Reception :
Intracellular receptors are found inside the cell,
either in the cytoplasm or nucleus of the target
cell. (The cell that is being signaled).
Small or hydrophobic chemical messengers,
such as steroid hormones, can attach to these
intracellular receptors by passing through the
plasma membrane unaided. The signal
molecule must bind to the active receptor
before it can be triggered to start a biological
reaction, such a change in gene expression.

10. Cells usually choose a multi-step pathway that transmits the signal quickly while amplifying it to
several molecules at each level because signaling systems must react quickly to tiny quantities of
chemical signals. Proteins are typically activated by the addition or removal of phosphate groups in
the signal transduction pathway. Enzymes called protein kinases are responsible for moving
phosphate groups from ATP to proteins. Protein kinases are common relay molecules in a signal
transduction pathway and regularly interact with one another.
This frequently causes a cascade of phosphorylation, in which one enzyme phosphorylates another,
which in turn phosphorylates a different protein. A significant part of the phosphorylation cascade
is played by the class of proteins known as protein phosphates. Protein phosphatases are enzymes
that swiftly dephosphorylate proteins (remove phosphate groups) and render protein kinases
inactive. Protein phosphatases serve as the signal transduction pathway's "off switch."The signal
transduction pathway must be disabled when the stimulus is no longer present in order to ensure
that the biological reaction is properly controlled. Protein kinases are also made available for reuse
via dephosphorylation, enabling the cell to react once more to fresh signals.
For the transmission of signals, cells require more than only kinases. Target molecules in the
cytoplasm or nucleus can receive signals from cell surface receptors via second messengers, which
are small, nonprotein, water-soluble molecules or ions (the ligand that binds the receptor is the first
messenger). Second messengers include calcium ions and cyclic AMP (cAMP).
Transduction :

11. In the end, cell signaling controls one or more cellular processes. Gene expression (the activation or
suppression of specific gene transcription) is commonly regulated by cell signaling. An ion channel in
the lasma membrane may open or close as a result of a signaling route, or a cell's metabolism may
change as a result of monitoring glycogen degradation. Significant biological processes like cell
division or death can also be influenced by signaling networks. (Cell death that is planned).
Response :

12. One of the most prevalent neurodegenerative disorders in the world is Alzheimer's disease. Clinically, it is distinguished
by intracellular neurofibrillary tangles and extracellular amyloid plaques, which cause neuronal malfunction and cell
death. The uneven processing of the amyloid precursor protein (APP) is a key feature of this illness. APP is a membrane
protein that is processed through proteolysis. The initial cleavage of APP by -secretase results in the production of sAPP
and a C83 carboyterminal fragment.
Normal synaptic signaling is linked to the existence of sAPP. It controls synaptic plasticity and neuronal survival, two
processes that support higher-order mental activities including memory and learning. As an alternative, -secretase and
-secretase may successively cleave APP to release extracellular monomers of various sizes, the most important of which
is A40/42.When a disease is present, an imbalance in the APP processing pathways causes neurotoxic monomers to
accumulate more frequently, resulting in A oligomerization and plaque formation.Ion channel blockade, calcium
homeostasis disruption, mitochondrial oxidative stress, poor energy metabolism, aberrant glucose control, altered
synaptic function, and finally neuronal cell death are all consequences of pathogenic A aggregation.
In the setting of amyloid monomer, oligomer, and plaque deposition, a number of glial cell types, including astrocytes
and microglia, have been identified as both neuroprotective and pathogenic. Neurofibrillary tangles, which are made of
hyperphosphorylated versions of the Tau protein coupled with microtubules, are another feature of Alzheimer's
disease.Other kinases like PKC, PKA, and Erk2 are also involved in the phosphorylation of Tau, although GSK-3/ and
CDK5 are the two main kinases that do it. When tau is overphosphorylated, it separates from the microtubule, which is
followed by microtubule instability and tau protein oligomerization, all of which contribute to the formation of
neurofibrillary tangles inside the cell. The neuron undergoes apoptosis as a result of the progressive accumulation of
these tangles.
Faulty Signaling Pathway :

13. What is the faulty
mechanism of
Alzheimer's disease?
A dysfunctional blood-brain barrier in an Alzheimer's
patient inhibits glucose from getting to the brain and
hinders the removal of harmful beta-amyloid and tau
proteins.
This causes inflammation, which exacerbates the
vascular issues in the brain.

14. Alzheimer's symptoms can differ from person to person. One of
the initial symptoms of the condition is frequently memory issues.
Alzheimer's may also be detected in its early stages by a
deterioration in non-memory components of cognition, such as
difficulty using the correct word, difficulty comprehending visual
imagery and spatial relationships, and impaired reasoning or
judgment. More severe symptoms, such as increased
disorientation and behavioral problems, appear as the condition
worsens.
The majority of Alzheimer's patients, particularly those with the
late-onset form, have early symptoms in their mid-60s or later.
Early-onset Alzheimer's, which can start as early as a person's 30s
but is uncommon, is the term for the illness when it manifests
before age 65.
Clinically, Alzheimer's normally develops in four stages: preclinical,
mild (also known as early-stage), moderate, and severe
(sometimes known as late-stage).
The cause and core
symptoms of Alzheimer's

15. Signs of Mild Alzheimer’s disease :
 daily life is disrupted by memory loss
 Poor decision-making due to poor judgment
 decline in initiative and spontaneity
Signs of moderate Alzheimer’s disease
 more confusion and memory loss, including
forgetting dates or past experiences.
 abandoning social activities.
 unable to pick up new skills.
Signs of severe Alzheimer's disease
 being unable to communicate.
 No understanding of the present situation or recent
events.
 Loss of weight without much appetite.

16. Due to the complexity of the condition, no one treatment or other
intervention will ever be able to fully address all cases of
Alzheimer's disease. Despite this, researchers have made
significant strides in recent years in better understanding
Alzheimer's disease and developing and evaluating novel
treatments, including a number of medications in advanced clinical
trials. Numerous prescription drugs have previously received FDA
approval to help treat the symptoms of Alzheimer's disease in
patients.
Additionally, on June 7, 2021, the FDA approved aducanumab, a
novel drug that helps to eliminate amyloid deposits in the brain
and may slow the progression of Alzheimer's. It has not yet been
demonstrated that it has an impact on clinical outcomes or
symptoms like dementia progression or cognitive decline. People
with early- or middle-stage Alzheimer's benefit the most from the
majority of treatments. It is crucial to remember that none of the
known treatments can reverse Alzheimer's disease.
How Is Alzheimer's
Disease Treated?

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