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Alzheimer's disease (AD) primarily affects AMPA and NMDA glutamatergic receptors, serotonergic 5-HT6 receptors, and cholinergic nicotinic and muscarinic receptors. The document discusses the relationship between AD and other conditions like cancer, hypertension, and stroke, highlighting common pathophysiological features and the increasing prevalence of dementia. Despite ongoing research, AD remains incurable, with projections indicating a significant rise in cases by 2050.

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Devansh Singh
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8 views

Document 2 (5)

Alzheimer's disease (AD) primarily affects AMPA and NMDA glutamatergic receptors, serotonergic 5-HT6 receptors, and cholinergic nicotinic and muscarinic receptors. The document discusses the relationship between AD and other conditions like cancer, hypertension, and stroke, highlighting common pathophysiological features and the increasing prevalence of dementia. Despite ongoing research, AD remains incurable, with projections indicating a significant rise in cases by 2050.

Uploaded by

Devansh Singh
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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What receptors are affected by alzheimer’s disease

The main receptors implicated in AD symptoms are the AMPA and NMDA glutamatergic receptors,
ionotropic and metabotropic receptors serotonergic 5-HT6 receptors and the cholinergic nicotinic
alpha7 and muscarinic M1 and M2 sub types
Applications of Alzheimer disease:
In cancer : Alzheimer’s disease (AD) and cancer are among the leading causes of human death around
the world. While neurodegeneration is the main feature of AD, the most important characteristic of
malignant tumors is cell proliferation, placing these two diseases in opposite sides of cell division
spectrum.
AD and cancer’s pathologies consist of a remarkable common feature and that is the presence of
active cell cycle in both conditions
As examples, the role of phosphoinositide 3 kinase/Akt/ mammalian target of rapamycin
(PI3K/Akt/mTOR) signaling pathway in cell cycle re-entry and blocking autophagy are discussed as
potential common intracellular components between AD and cancer pathogenesis, with diverse
clinical diagnosis.
Beta amyloid hypothesis, however, was challenged when the presence of senile plaques were
reported in normal subjects with no clinical symptoms of AD.
In hypertension : Alzheimer disease (AD) is the most common cause of dementia with the
devastating consequences that everyone is aware of.1 There are 2 forms of AD: first, the familial AD
represents <2% of the cases; it is inherited in an autosomal dominant pattern with symptoms typically
presenting as early as 24 years of age for the most aggressive familial AD mutation identified to date,
the Leu to Pro mutation at position 166 of presenilin-1
AD pathology is confirmed postmortem by the accumulation of extracellular amyloid-β (Aβ)
containing plaques and intracellular neurofibrillary tau tangles in the brain.3 Proteolytic γ-secretase
presenilin-1 and -2 generate the amyloidogenic Aβ peptides. Although various Aβ peptide lengths are
produced by γ-secretase, Aβ42 and Aβ40 are of particular interest because the additional 2
hydrophobic residues in Aβ42 increase its ability to aggregate, providing the scaffold for oligomeric
and fibrillar forms of Aβ.2 The possible causal role of Aβ in AD is supported by the fact that a high
Aβ42 to Aβ40 ratio is an important determinant for the onset of amyloid pathology in familial AD.
Alzheimer’s disease (AD) is the most common form of dementia. Up to date AD cannot be prevented,
slowed or cured. As a consequence, both industrial and developing countries are facing an epidemic
crisis given that the number of cases would double every 20 years. By 2050, it is estimated that 115.4
million people will be affected by dementia [1]. For a century now, AD has been considered as a
purely neurodegenerative disease even though a vascular component of the disease was put forward
at its first description: AD was first described by Alois Alzheimer, an expert of vascular dementia [2],
who thought AD to be caused partly by vascular malfunction [3,4]. The autopsy of Auguste D’s [5]
brain revealed what will become the hallmarks of the disease: the senile plaques (SPs) and the
neurofibrillary tangles (NFT).
In stroke : A neurodegenerative disorder, Alzheimer's disease (AD), is characterized by dementia in
which there is an age-related decline in cognition and higher functions. Stroke is a cerebrovascular
disorder that frequently presents in old age and is a known risk factor for AD development. However,
the association that AD can be a risk factor for stroke is not well-studied. This review article compiled
various studies that pointed out the association between stroke development in patients with
dementia, particularly AD-related dementia. The pathophysiological progression of stroke in AD cases
and the genetic makeup possibly affecting the interrelation between these disorders were analyzed in
detail using currently available data and studies.
The pathophysiological progression of stroke in AD cases and the genetic makeup possibly affecting
the interrelation between these disorders were analyzed in detail using currently available data and
studies. Therapeutic and management modalities already in use for AD were put together, and the
possibility of early intervention in such patients benefiting cerebrovascular pathologies, particularly
stroke-related, was explored. Prognostic differences between patients of stroke with and without AD
were also reviewed, and how appropriate management can reduce the burden on health care settings
when both present simultaneously was emphasized.

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