Authors :
Sujay Vipin Katoch
Volume/Issue :
Volume 9 - 2024, Issue 9 - September
Google Scholar :
https://tinyurl.com/45ddrpk8
Scribd :
https://tinyurl.com/ys9y5756
DOI :
https://doi.org/10.38124/ijisrt/IJISRT24SEP629
Note : A published paper may take 4-5 working days from the publication date to appear in PlumX Metrics, Semantic Scholar, and ResearchGate.
Abstract :
Neurodegenerative diseases (NDDs) include
Alzheimer's disease, Parkinson's disease, Amyotrophic
Lateral Sclerosis (ALS), Huntington's Disease, and Pick's
disease. These conditions are characterized by a
progressive decline in the structure and function of the
nervous system. The objective of this paper is to provide
a brief overview of these diseases, outline the anatomical
changes they cause in the brain, and evaluate the level of
public awareness about their prevalence and impact.
Neuroimaging studies show that Alzheimer's disease
initially leads to the degeneration of neuronal connections
in brain regions associated with memory, such as the
entorhinal cortex and hippocampus. ALS is characterized
by the degradation of motor neurons in the spinal cord
and brainstem, leading to muscle weakness and atrophy.
In contrast, Parkinson's disease involves the decay of
dopaminergic neurons in the substantia nigra, resulting in
motor control impairments. Brain structure changes are
linked to the accumulation of abnormal protein
aggregates such as amyloid beta in Alzheimer's disease
and alpha-synuclein in Parkinson's disease, interfering
with cellular functions and causing neuronal death.
Besides addressing brain structure, this paper presents
results from a survey assessing public awareness of
neurodegenerative diseases. The findings suggest that
while the public is well-informed about Alzheimer's and
Parkinson's disease, there is still a significant knowledge
gap regarding less common conditions like ALS and
Huntington's disease. The significance of implementing
thorough educational approaches to increase public
knowledge is highlighted by these results. This study seeks
to narrow the divide between scientific knowledge and
public awareness of neurodegenerative diseases by
combining anatomical understanding with public
perceptions.
Keywords :
Neurodegenerative Diseases, Tauopathy, Anatomical Changes, Awareness, Integrating Anatomical Insights with Public Perceptions.
References :
- Peter R Mouton, Lee J Martin, Michael E Calhoun, Gloria Dal Forno, Donald L Price, Cognitive decline strongly correlates with cortical atrophy in Alzheimer’s dementia, Neurobiology of Aging, Volume 19, Issue 5, 1998.
- Kosaka K, Ikeda K, Kobayashi K, Mehraein P (1991) Striatopallidonigral degeneration in Pick’s disease: a clinicopathological study of 41 cases. J Neurol 238: 151-160
- Hulette CM, Crain BJ (1992) Lobar atrophy without Pick bodies. Clin Neuropathol 11: 151-6
- Clark AW, Manz HJ, White CL III, Lehmann J, Miller D, Coyle JT (1986) Cortical degeneration with swollen chromatolytic neurons: its relationship to Pick’s disease. J Neuropathol Exp Neurol 45: 268-284
- Williams HW (1935) The peculiar cells of Pick’s disease: Their pathogenesis and distribution in disease. Arch Neurol Psychiatry 34: 508-519
- Yoshimura N (1989) Topography of Pick body distribution in Pick’s disease: a contribution to understanding the relationship between Pick’s and Alzheimer’s diseases. Clin Neuropathol 8: 1-6
- Hof PR, Bouras C, Perl DP, Morrison JH (1994) Quantitative Neuropathologic analysis of Pick’s disease cases: cortical distribution of Pick bodies and coexistence with Alzheimer’s disease. Acta Neuropathol 87: 115-124
- Dickson, D. W. (1998). Pick's disease: a modern approach. Brain pathology, 8(2), 339-354.
- Davis DG, Wang HZ, Markesbery WR (1992) Image analysis of neuropil threads in Alzheimer’s Pick’s diffuse Lewy body disease and in progressive supranuclear palsy. J Neuropathol Exp Neurol 51: 594-600
- Cochran EJ, Fox JH, Mufson EJ (1994) Severe panencephalic Pick’s disease with Alzheimer’s disease-like neuropil threads and synaptophysin immunoreactivity. Acta Neuropathol 88: 479-484
- Jones L. The cell biology of Huntington’s disease. In: Bates G, Harper P, Jones L, eds. Huntington’s disease. New York: Oxford University Press, 2002: 348–62.
- Saudou F, Finkbeiner S, Devys D, Greenberg ME. Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions. Cell 1998; 95: 55–56.
- Peter MF, Nucifora FC Jr, Kushi J, et al. Nuclear targeting of mutant Huntingtin increases toxicity. Mol Cell Neurosci 1999; 14: 121–81.
- Wellington CL, Leavitt BR, Hayden MR. Huntington disease: new insights on the role of huntingtin cleavage. J Neural Transm Suppl 2000; 58: 1–17
- Lunkes A, Mandel JL. A cellular model that recapitulates major pathogenic steps of Huntington’s disease. Hum Mol Genet 1998; 7: 1355–61.
- The Huntington’s Disease Collaborative Research Group. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington’s disease chromosomes. Cell 1993; 72: 971–83.
- Mukai H, Isagawa T, Goyama E, et al. Formation of morphologically similar globular aggregates from diverse aggregation-prone proteins in mammalian cells. Proc Natl Acad Sci USA 2005; 102: 10887–92.
- Rangone H, Humbert S, Saudou F. Huntington’s disease: how does huntingtin, an anti-apoptotic protein, become toxic? Pathol Biol 2004; 52: 338–42.
- Rubinsztein DC. Molecular biology of Huntington’s disease (HD) and HD-like disorders. In: Pulst S, ed. Genetics of movement disorders. California: Academic Press, 2003: 365–77.
- Bates GP, Benn C. The polyglutamine diseases. In: Bates G, Harper P, Jones L, eds. Huntington’s disease. New York: Oxford University Press, 2002: 429–74.
- Mills IG, Gaughan L, Robson C, et al. Huntingtin interacting protein 1 modulates the transcriptional activity of nuclear hormone receptors. J Cell Biol 2005; 170: 191–200
- Cha JH. Transcriptional dysregulation in Huntington’s disease. Trends Neurosci 2000; 23: 387–92.
- Hickey MA, Chesselet MF. Apoptosis in Huntington’s disease. Prog Neuropsychopharmacol Biol Psychiatry 2003; 27: 256–65.
- Panov AV, Burke JR, Strittmatter WJ, Greenamyre JT. In vitro eff ects of polyglutamine tracts on Ca2+-dependent depolarization of rat and human mitochondria: relevance to Huntington’s disease. Arch Biochem Biophys 2003; 410: 1–6
- Bae BI, Xu H, Igarashi S, et al. P53 mediates cellular dysfunction and behavioral abnormalities in Huntington’s disease. Neuron 2005; 47: 29–41.
- DiProspero NA, Chen EY, Charles V, Plomann M, Kordower JH. Early changes in Huntington’s disease patient brains involve alterations in cytoskeletal and synaptic elements. J Neurocytol 2004; 33: 517–33.
- Modregger J, DiProspero NA, Charles V, Tagle DA, Plomann M. PACSIN 1 interacts with huntingtin and is absent from synaptic varicosities in presymptomatic Huntington’s disease brains. Hum Mol Genet 2002; 11: 2547–58.
- Freeman W, Morton AJ. Regional and progressive changes in brain expression of complexin H in a mouse transgenic for the Huntington’s disease mutation. Brain Res Bull 2004; 63: 45–55.
- Charrin BC, Saudou F, Humbert S. Axonal transport failure in neurogenerative disorders: the case of Huntington’s disease. Pathol Biol 2005; 53: 189–92.
- Zuccato C, Liber D, Ramos C, et al. Progressive loss of BDNF in a mouse model of Huntington’s disease and rescue by BDNF delivery. Pharmacol Res 2005; 52: 133–39.
- Gauthier LR, Charrin BC, Borrell-Pages M, et al. Huntingtin controls neurotrophic support and survival of neurons by enhancing BDNF vesicular transport along microtubules. Cell 2004; 118: 127–38.
- Busch A, Engemann S, Lurz R, et al. Mutant huntingtin promotes the fibrillogenesis of wild-type huntingtin: a potential mechanism for loss of huntingtin function in Huntington’s disease. J Biol Chem 2003; 278: 41452–61.
- Pulst SM, Nechiporuk A, Nechiporuk T, et al. Moderate expansion of a normally biallelic trinucleotide repeat in spinocerebellar ataxia type 2. Nat Genetics 1996; 14: 237–38.
- Komure O, Sano A, Nishino N, et al. DNA analysis in hereditary dentatorubral-pallidoluysian atrophy: correlation between CAG repeat length and phenotypic variation and the molecular basis of anticipation. Neurology 1995; 45: 143–49.
- Halliday GM, McRitchie DA, Macdonald V, Double KL, Trent RJ, McCusker E. Regional specificity of brain atrophy in Huntington's disease. Exp Neurol. 1998 Dec;154(2):663-72. doi: 10.1006/exnr.1998.6919. PMID: 9878201.
- Parekh, N., Bhagat, A., Raj, B. et al. Artificial intelligence in diagnosis and management of Huntington’s disease. Beni-Suef Univ J Basic Appl Sci 12, 87 (2023).
- Yale Medicine, Huntington's Disease, Fact sheet
- Stoker TB, Mason SL, Greenland JC, et al, Huntington’s disease: diagnosis and management, Practical Neurology 2022;22:32-41.
- Nature,28/07/2024, [https://www.nature.com/]
- UtDallas,08/08/2024, [https://www.utdallas.edu/]
- Docplayer,12/08/2024, [https://docplayer.net]
- Walker, F. O. (2007). Huntington's disease. The Lancet, 369(9557), 218-228.
- Researchgate,23/08/2024, [https://www.researchgate.net/ ]
- Coursehero,23/08/2024, [https://www.coursehero.com/]
- UCLA,25/08/2024, [brainpath.medsch.ucla.edu]
- UMDNJ, 26/08/2024, [www2.umdnj.edu]
- NLM,26/08/2024, [https://www.ncbi.nlm.nih.gov/]
- Blackhurst, B.M., Funk, K.E. Viral pathogens increase risk of neurodegenerative disease. Nat Rev Neurol 19, 259–260 (2023). https://doi.org/10.1038/s41582-023-00790-6
Neurodegenerative diseases (NDDs) include
Alzheimer's disease, Parkinson's disease, Amyotrophic
Lateral Sclerosis (ALS), Huntington's Disease, and Pick's
disease. These conditions are characterized by a
progressive decline in the structure and function of the
nervous system. The objective of this paper is to provide
a brief overview of these diseases, outline the anatomical
changes they cause in the brain, and evaluate the level of
public awareness about their prevalence and impact.
Neuroimaging studies show that Alzheimer's disease
initially leads to the degeneration of neuronal connections
in brain regions associated with memory, such as the
entorhinal cortex and hippocampus. ALS is characterized
by the degradation of motor neurons in the spinal cord
and brainstem, leading to muscle weakness and atrophy.
In contrast, Parkinson's disease involves the decay of
dopaminergic neurons in the substantia nigra, resulting in
motor control impairments. Brain structure changes are
linked to the accumulation of abnormal protein
aggregates such as amyloid beta in Alzheimer's disease
and alpha-synuclein in Parkinson's disease, interfering
with cellular functions and causing neuronal death.
Besides addressing brain structure, this paper presents
results from a survey assessing public awareness of
neurodegenerative diseases. The findings suggest that
while the public is well-informed about Alzheimer's and
Parkinson's disease, there is still a significant knowledge
gap regarding less common conditions like ALS and
Huntington's disease. The significance of implementing
thorough educational approaches to increase public
knowledge is highlighted by these results. This study seeks
to narrow the divide between scientific knowledge and
public awareness of neurodegenerative diseases by
combining anatomical understanding with public
perceptions.
Keywords :
Neurodegenerative Diseases, Tauopathy, Anatomical Changes, Awareness, Integrating Anatomical Insights with Public Perceptions.